Journées de l’Ecole Doctorale
Physiologie, Physiopathologie et Thérapeutique
Centre de Recherche des Cordeliers
25th and 26th
May, 2016
ACKNOWLEDGMENTS
The organizers would like to thank the following sponsors and exhibitors for their
time and financial support.
The Organizers would also like to thank all of the chairmen and chairwomen, the
conference speakers, and the jury members, for their implication and essential
presence, and for inspiring us with professionalism.
Our warmest thanks also to the Doctoral School’s directors, Pr. Isabelle Cremer
and Dr. Catherine Monnot and the administrator, Mrs Dominique Belle, for their
guidance and unwavering support.
SCIENTIFIC PROGRAM
Wednesday, 25th May, 2016
8:30-9:00 WELCOMING OF PARTICIPANTS
9:00-9:15 INTRODUCTION
Pr. Isabelle CREMER - ED394 director
Dr. Catherine MONNOT - ED394 deputy director
9:15-10:15 PLENARY SESSION I: ONCOLOGY Chair: Yann-Alexandre VANO - Georges Pompidou European Hospital
Adem BOKHARI (UMRS 938, Saint-Antoine Hospital) - Aberrant Splicings due to
Microsatellite Instability in Cancer: Physiopathological role of HSP110 mutation in
colorectal cancer
Benoît USUNIER (IRSN) – Mesenchymal stem cell therapy reduces fibrosis induced
by abdomino-pelvic radiotherapy
Marion CLASSE (Pitié Salpêtrière Hospital) - Molecular characterization of olfactory
neuroblastomas
Maurice ZAOUI (UMRS 938 - UPMC) - Reciprocal changes in gene expression
profiles of cocultured breast cancer cells and adipocytes
10:15 -10:30 POSTER TEASING – FIRST SESSION
10:30 -11:45 POSTER PRESENTATION (1ST SESSION) / Coffee break and Sponsors' visit
11:45 -12:45 PLENARY SESSION II: NEUROLOGY & VISION Chair: Gaël ORIEUX - Institut de la Vision
Hugo CHARLES-MESSANCE (UMRS 968 - Institut de la Vision)
Mononuclear phagocytes induce IL-1β dependent photoreceptor toxicity
Linda HANBOUCH (UMRS 1127 - Institut du Cerveau et de la Moelle)
Mutations at the cholesterol binding site on Amyloid precursor protein modifies
the secretion of amyloid peptides from transfected HEK293T cells
Emily QUENTIN (UMRS 839 - Institut du Fer à Moulin)
CIPPscaffoldprotein :anewinteractorofC-terminal5-HT2Bserotonergic
receptorpromotesignalingpathwayactivity
Emilie SIMONNET (Collège de France) - RoleofEphrine-A4 in the development
and in the physiology of arterial innervation
12:45-14:00 LUNCH BREAK AND SPONSORS’ VISIT
14:00-15:15 LIVE ROUND TABLE DISCUSSION “SCIENTIFIC COMMUNICATION” (French language / en français) Ange ANSOUR – Educational Coordinator “Les Savanturiers”
Mathieu BUONAFINE – Winner of “My Thesis in 180 Seconds”
Anne NASSIF – "Nutrimedia" director
Séverine CIANCIA – Head of Press Inserm Service
Noémie NAGUET – "l'Esprit Sorcier" ("C'est pas sorcier" new version)
15:15-15:30 POSTER TEASING – SECOND SESSION
15:30-16:45 POSTER PRESENTATION (2ND SESSION) / Coffee break and Sponsors' visit
16:45-18:30 PLENARY SESSION III: PATHOPHYSIOLOGY
Chairs: Philippe LE ROUZIC - Saint-Antoine & Gilles CRAMBERT – CRC Mathieu BUONAFINE (UMRS 1138 - CRC) – Implication of the Neutrophil
Gelatinase-Associated Lipocalin (NGAL) from immune cells in aldosterone
induced cardiovascular remodeling
Olivier CLAUDE (UMRS 1166 - ICAN) – Identification of selective adult cardiac
progenitor cells (CPCs) surface markers by proteogenomics approaches
Irma Karen LOPEZ CAYUQUEO (UMRS 970) - Knockin of HA-tagged K+ channel
Kir7.1 as a tool to determine its segmental and subcellular localisation in mouse
kidney.
Ahmad MASSARWEH (UMRS 1149 - UPMC) – Golgi Dolichol linked Oligosaccharide
(DLO) Diphosphatase, a potential regulator of DLO metabolism
Meriam NEFLA (UMRS 938 - Saint-Antoine) – The proinflammatory cytokine 14-3-3ε
is a ligand of CD13 in cartilage.
Benjamin VALLIN (UMRS 8256 - UPMC) – Identification of a new adenylyl cyclase 8
(AC8) isoform: implication in vascular smooth muscle cells (VSMCs)
transdifferentiation and pathological vascular remodeling
Thursday, 26th May, 2016
9:00-10:00 PLENARY SESSION IV: IMMUNOLOGY & INFLAMMATION Chair: Catherine SAUTÈS-FRIDMAN – CRC
Mélanie CRON (UMRS 974 - Pitié-Salpêtrière Hospital) – Characterization of the role
of miR-150 in autoimmune Myasthenia Gravis
Clément LEVIN (CIMI - Pitié-Salpêtrière Hospital) – Role of skin migratory antigen-
presenting cells in T follicular helper cell polarization after intradermal vaccination
Anastasia MIKHAILOVA (Institut Pasteur) – The role of Tuba protein in the dynamics
of immune synapse formation
Emmanuel STEPHEN-VICTOR (UMRS 1138 - CRC) - Cellwallα-(1,3)-glucanfrom
Aspergillus fumigatus induces PD-L1 expression on human dendritic cells that
regulates Th1 and regulatory T cell responses
10:00-10:15 POSTER TEASING – THIRD SESSION
10:15-11:30 POSTER PRESENTATION (3RD SESSION) / COFFEE BREAK AND SPONSORS' VISIT
11:30-12:30 PLENARY SESSION V: VIROLOGY Chair: Olivier SCHWARTZ – Institut Pasteur
Iratxe DEL RIO (Institut Pasteur) - HIV-1 modulation of the T cell activation
molecular machinery
Olivier LUCAR (CIMI - Pitié-Salpêtrière) – New Family of Neutralizing Antibodies in
HIV Asymptomatic Long-Term Non-Progressors
Angeline ROUERS (CIMI - Pitié-Salpêtrière Hospital) – Follicular helperT cells (Tfh)
and memory B cell response during HIV-1 infection
Zineb SBIHI (CIMI - Pitié-Salpêtrière Hospital) – iNKT and Memory B cells deficiency
in HHV-8 Multicentric Castleman Disease
12:30-14:00 LUNCH BREAK AND SPONSORS’ VISIT
14:00-15:00 “SCIENTIFIC INTEGRITY” LECTURE BY PR. PIERRE CORVOL
(French language / en français)
15:00-16:00 PLENARY SESSION VI: METABOLISM & NUTRITION
Chairs: Ghislaine GUILLEMAIN & Armelle LETURQUE – CRC Mengyue HU (UMRS 1138 - CRC) - The role of receptor activator of NF-kB (RANK)
and its ligand (RANKL) in the Non-Alcoholic Fatty Liver Disease(NAFLD)
Cécilia LANDMAN (UMRS 1157 - UPMC) – The N-acyl-homoserine lactone 3-oxo-
C12, an inter-bacterial signaling molecule (involved in quorum sensing), exerts
effects on the host: thus implicating quorum sensing in Inflammatory Bowel
Disease
Ludovica MARINELLI (FInE team - MICALIS, INRA Jouy-en-Josas) - Activation of the
AhR signal pathway by the gut microbiota
Hedi SOUSSI (UMRS 1166 - ICAN) – DAPK2 down-regulation associates with
attenuated adipocyte autophagic clearance in human obesity
16:00-16:15 POSTER TEASING – FOURTH SESSION
16:15-17:30 POSTER PRESENTATION (4TH SESSION), COFFEE BREAK AND SPONSORS' VISIT
17:30-19:00 CLOSING CEREMONY OF THE 17TH JEDS AND AWARDING OF THE PARTICIPANTS -
COCKTAIL
ORAL COMMUNICATIONS - 25th May 2016
Oncology
Adem BOKHARI, Ada Collura, Alex Duval - Aberrant Splicings due to Microsatellite
Instability in Cancer : Physiopathological role of HSP110 mutation in colorectal cancer.
UMRS 938, Saint-Antoine Hospital
Microsatellite instability (MSI) results from impaired DNA mismatch repair, being associated with a
frequent subset of human neoplasms. In the lab, we recently identified the first mutation
affecting a chaperone in human cancer. MSI affects a T17 intronic DNA repeat, located in the
splice acceptor site of HSP110 intron 8 in MSI colorectal cancer (CRC) and leads to aberrant
skipping of exon 9 and the apparition of a premature codon stop (PTC) in the exon 10, resulting
of a mutant protein, referred to as HSP110DE9. We demonstrate that HSP110DE9 interacts with
wild-type HSP110, antagonizing its chaperone activity (dominant negative effect). Moreover, the
overexpression of HSP110DE9 increases the sensitivity of CRC cells to anti-cancer agents and
HSP110 T17 status predicts the relapse-free survival of MSI CRC patients treated with adjuvant
chemotherapy.
In line with these results, the first axis of my PhD project focus to investigate the
pathophysiological consequences of HSP110 mutation in CRC. In our work, now submitted, we
reported that HSP110 induces colon cancer cell proliferation via STAT3 activation, specifically an
increase in STAT3 phosphorylation, nuclear translocation and transcription factor activity. Thus,
the frequent inactivating mutation of this chaperone is probably an important event underlying
the improved prognosis of colon cancer displaying MSI.
In a second work in progress to submission, we study the NMD (Nonsense-mediated mRNA
decay) system as a therapeutical target for MSI CRC. NMD is responsible for the degradation of
mutant mRNAs containing a PTC. We hypothesized that inhibition of NMD activity could be of
particular therapeutic interest for MSI tumors leading to increase of HSP110DE9 protein level.
Using Amlexanox, an approved drug used in clinic, we were able to block the degradation of
HSP110DE9 transcript. Interestingly, systemic administration of this drug led to growth inhibition of
MSI CRC xenografts, but not of microsatellite stable.
Benoît USUNIER, BrunoL’Homme,RadiaTamarat,MarcBenderitterand AlainChapel
– Mesenchymal stem cell therapy reduces fibrosis induced by abdomino-pelvic
radiotherapy.
InstituteofRadiologicalProtection and Nuclear Safety, RadioProtection and Human Health Division,
Fontenay-aux-Roses, France
Theabdomino-pelvicareacontainsthemainorgansatriskforcancer (prostate, colon-
rectum, cervix…). Treatmentprotocolsofteninclude radiotherapy which, while effective for
sterilization of thetumor, cancauseseverelatecomplications, such as fibrosis. During such
treatment, colon andrectumareespecially susceptible to side effects, due to their rapid self-
renewal. There currentlyexistsnoreliabletherapy against fibrosis. Seeinghow Mesenchymal
Stem Cell (MSC) hasproveneffectivein treating radiation injuries, weaimed at
investigatingtheir abilityto reduce radiation-inducedfibrosis to thecolon and rectum. Invivo,
weevaluatedthe effectsofMSC transplantationin rats. We usedasingle dose 29 Gy
colorectal irradiation model on Sprague-Dawley rats. This model produces damages similar
tothelate severelesions observed inradiotherapy patients. MSCswere injected intravenously
atdifferenttime points after radiationexposure to studytheefficacy of cell therapy
priorandafter fibrosisonset. MSCs wereable to reduce fibrosisinboth these situations,
mainlythroughthe inhibitionof inflammatory pathways and thereduction of myofibroblast
activation.Keymediators ofthe effect ofMSCshavebeen identified during this study.
Themodificationofmacrophage polarization towards theM2 phenotypeis induced by
MSCsin vivoand appears to play a major role in their antifibrotic effects. To further understand
the mechanisms underlyingtheseeffects, wesetupna invitro model of myofibroblast
activation. Intestinalfibroblasts andsmooth muscle cells, themainpro-fibrotic cells
inthecolon, were irradiated toinduce changes similar to thoseobservedinvivo. When
cocultured with MSCs, we observed adecreaseinprofibrotic proteins secretionbythese cells.
TheseresultssuggestthatMSC therapyrepresents a promising strategyin the treatment
ofsevereenteritis, rectitisinducedbyradiotherapy of prostate, bladder,uterus cancers.
Marion CLASSE1-3, Xaoping Su2, Michel Wassef3, Frederic Allanic1, Roger Mouawad1,
Benjamin Verillaud4, Geoffrey Mortuaire5, Philippe Herman4, Gabriel Malouf1 and David
Khayat1 - Molecular characterization of olfactory neuroblastomas. 1Département d’ Oncologie Médicale, Groupe Hospitalier Pitiié Salpêtrière, Assistance Publique Hôpitaux
de Paris, Faculté de Médecine Pierre et Marie Curie, Institut Universitaire de Cancérologie GRC5, Université
Paris 6, Paris, France. 2Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer
Center, Houston, Texas, USA. 3Département de Pathologie, Hôpital Lariboisière, Assistance Publique Hôpitaux de Paris, Paris, France. 4Département de chirurgie ORL, Hôpital Lariboisière, Assistance Publique Hôpitaux de Paris, France 5Département de chirurgie ORL, CHRU de Lille, France.
Background: olfactory neuroblastomas (ONBs) are rare tumors arising in the skull base, thought
to develop from neuronal or basal cells of olfactory mucosa. They are traditionally classified into
4 grades according to Hyams grading system which is subjective and poorly reproducible.
Recent studies suggest a simplified classification into low and high grade but no objective
argument has been proved. The goal of our work was to determine a molecular profile of ONBs
compared to normal sinonasal mucosa and to other sinonasal cancers, in order to confirm their
nature and to highlight objective elements to draw the foundations of a new classification
system.
Materiel and methods: we performed RNA next-generation sequencing on 18 ONBs, 1 sinonasal
neuroendocrine carcinoma (SNEC), 3 squamous cell carcinomas (SCCs), 3 intestinal type
adenocarcinomas (ITACs) and 4 normal sinonasal mucosa cryopreserved samples retrieved
from Lariboisière-APHP and Lille-CHRU Pathology departments. All cases were reevaluated and
reclassified if necessary by 2 pathologists.
Results: Unsupervised clustering of gene expression revealed 2 groups. The first group was
composed of normal samples which clustered together, SCCs and ITACs which clustered
according to their histological type and 1 ONB which clustered with SCCs. The second group
was composed of ONBs and the SNEC. Two sub-groups of ONBs were identified. Some of the
most differently overexpressed RNAs in ONBs compared to carcinomas were related to neuronal
differentiation and AKT signaling pathway.
Conclusion: RNA sequencing proves ONBs have a gene expression profile very different from
sinonasal carcinomas and confirms their neuronal differentiation. It also brings molecular
elements to support a low grade – high grade distribution of ONBs. Closer analysis of the 2 ONBs
gene expression subgroups will highlight potential immunohistochemical and therapeutic targets
in order to improve diagnostic and classification, and open new therapeutic paths.
Maurice ZAOUI1,2,3, Nathalie Ferrand1,2,3, Annette K. Larsen1,2,3, Véronique Béréziat1,2,4
and Michèle Sabbah1,2,3 - Reciprocal changes in gene expression profiles of cocultured
breast cancer cells and adipocytes. 1UPMC Univ Paris 06, UMR-s 938, F-75005, Paris, France, 2INSERM UMR_S 938, Centre de recherche Saint-
Antoine, Paris, France. 3Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris,
France. 4Genetics and acquired lipodystrophies, Centre de Recherche Saint-Antoine, Paris, France.
Breast cancer is a frequent disease, affecting about one woman out of eight at some time of
life. Epidemiologic data have shown a strong correlation between obesity and increased risk of
breast cancer. Until now, little attention has been paid to the surrounding adipose tissue,
although recent data suggest for instance that adipocytes, under the influence of tumor cells
factors, can contribute to different stages of carcinogenesis. A critical step in tumor growth and
metastasis is tumor vascularization through angiogenesis pathway, which can be activated
directly or under hypoxic circumstances.
We first characterize, as a function of adipocyte stroma modifications, the vasculogenic profile
of epithelial or mesenchymal breast cancer cells. Then the influence of the adipocytes on this
vasculogenic profile.
The studies were conducted using Transwell where murine adipocyte cell line 3T3F442A were not
in direct contact with epithelial (MCF-7) or a mesenchymal (MCF7-sh-WISP2) breast cancer cell
lines . Then the genes and proteins expression levels of vasculogenic and hypoxic factors were
analyzed by QRT-PCR, Western-Blot and ELISA.
First, we observed different angiogenic profile between the epithelial and mesenchymal cell
lines. The MCF-7 cells showed a low VEGF-A, VEGF-C and NRP-1 expression while the
mesenchymal variant presented high levels of these factors. We compared the expression of HIF
(Hypoxia Induced Factor) and we found that mesenchymal cells expressed a higher level of
HIF1α but a lower of HIF1β compared to epithelial cells.
We then observed an increase of VEGF-A and VEGF-C secretion in both tumoral cell lines when
cocultured with adipocytes, while NRP-1 seemed unaffected. There was no effect when the
tumoral cells were cocultured with preadipocytes.
These data suggest that adipocytes can increase angiogenic properties of breast tumoral cells
by increasing their secretion of VEGF-A and VEGF-C leading to a more invasive and metastatic
tumor phenotype.
Neurology & Vision
Hugo CHARLES-MESSANCE1, Chiara Eandi1,2, Lourdes Siqueiros1,Alvaro Rendon1, Ramin
Tadayoni1,3, Florian Sennlaub1 and Xavier Guillonneau1 - Subretinal mononuclear
phagocytes induce IL-1β dependent photoreceptor toxicity 1SorbonneUniversités,UPMCUnivParis06,INSERM,CNRS,Institutdela Vision, 17 rue Moreau, 75012,
Paris, France 2UniversityofTorino, DepartmentofClinicalPhysiopathology,EyeClinic, Torino, Italy 3Serviced'Ophtalmologie,HôpitalLariboisière,AP-HP,DiderotUnivParis 07, Sorbonne Paris Cité, 2 rue
Ambroise Paré,75010,Paris,France
Age-related macular degeneration (AMD) is the leading cause of vision impairment in elderly: it
ischaracterizedbythedegenerationofthe photoreceptor cells in the macula, resulting
inaprogressivelossofcentral vision. AMD is associated with an infiltration and
chronicsubretinal accumulation of mononuclear phagocytes (MPs), among which monocytes
(Mos) andmicroglialcells.WehavepreviouslyshowninanAMDmodelthat subretinal
MosproduceIL-1βandthatIL-1βplaysakeyrolein Cx3cr1-/- Mos photoreceptor
(PR)toxicity.Tofurtherunderstandtherole ofIL-1β inPRtoxicity, we cultured mice retina in
thepresenceofIL-1βor Mos.After18hofculture, explantswere fixed and submitted to
TUNEL labelling or immunostained to label cone PR outer segment. We show that exogenous IL-
1β induced rod PR cell death and that antagonizing glutamate receptor reduces
rodPRcelldeath.InthepresenceofIL-1β, the number of cone PR was not affected
butastrongconesegmentlosswas observed. Similar results have been successfully
reproducedbyculturing retinalexplants with human or Cx3cr1-/- Mos. Our results indicatethat
subretinalMPs inducesevereIL-1β dependent rod and cone toxicity. We will further decipher
the molecular mechanism by which IL-1β impaired photoreceptor functions.
Linda HANBOUCH1, Catherine Marquer1, Gaëlle Fontaine1, Julien Moreau2, Nicolas Gilles3,
Caroline Louis4, Mark J. Millan4 and Marie-Claude Potier1 - Mutations at the cholesterol binding
site on Amyloid precursor protein modifies the secretion of amyloid peptides from transfected
HEK293T cells 1Institut du Cerveau et de la Moelle (ICM), CNRS UMR7225, INSERM UMR_S1127, UPMC, Hôpital Pitié-Salpêtrière, 47, Bd de
l’Hôpital 75013 Paris, France; 2Laboratoire Charles Fabry, Institut d’Optique Graduate School, Université Paris Sud, 2 avenue Augustin Fresnel, 91127
Palaiseau France; 3Centre de recherche du CEA/DSV/iBiTec-S/SIMOPRO Toxins, Receptors and Channels team. Saclay, Bat 152,91191 Gif
sur Yvette; 4Pôle d'Innovation Thérapeutique en Neuropsychiatrie, Institut de Recherches Servier, 125 chemin de Ronde, 78290
Croissy-sur-Seine France
Cholesterol levels are elevated in the brains of Alzheimer’s disease (AD) patients. An increase in
cholesterol at the plasma membrane promotes an increase of endocytosis of the amyloid
precursor protein (APP) leading to an increase of Aβ production. Moreover, an interaction
between C99, the protein fragment resulting from the cleavage of APP by BACE1, and
cholesterol has recently been described. In the present work, we studied the involvement of the
cholesterol-binding site (CBS) on APP endocytosis and the production of amyloid-β peptides
(Aβ).
Mutants of the CBS on APP751-mCherry were constructed using site-directed mutagenesis:
E693K, S697A, K699A, K699E, G700A, G704A, V710A, S697A/K699A and G700A/G704A (numbering
APP770). HEK293T cells were transfected with these mutants and the amounts of intracellular and
extracellular Aβ peptides were measured using ELISA and the MesoScale Discovery 24 hours
after transfection. In parallel, immunostaining of EEA1, a marker of early endosomes, was
performed to quantify the number and size’s endosomes. Surface Plasmon Resonance (SPR) was
used to quantify the interaction between 25aa peptides corresponding to wild-type (wt) or
mutated APP CBS and liposomes containing cholesterol.
All mutants, except S697A, produced very low levels of secreted Aβ40 and Aβ42 in HEK293T cells
as compared to wt (2.5 to 10 fold). Levels of Aβ40 were significantly lower with only three
mutants: K699A, V710A and S697A/K699A (3.2, 2.6 and 3.5 fold less respectively). Cells expressing
the mutant E693K showed an increase of the number and size’s endosomes. Cholesterol-loaded
liposomes and non-mutated wt peptides corresponding to the CBS of APP showed a significant
interaction whereas mutant peptides did not.
These results suggest that a specific interaction between the CBS of APP and cholesterol
modulates the secretion of Aβ40 and Aβ42. Furthering our understanding of the interaction
between cholesterol and APP could reveal novel therapeutic strategies for the treatment of
sporadic AD.
Emily QUENTIN1, ImaneMoutkine1, Sabine Levi1, Philip Marin2, Luc Maroteaux1 - CIPP
scaffold protein: a new interactor ofC-terminal5-HT2B serotonergic receptor promote
signaling pathway activity 1U INSERM 839, 2IGF Montpellier
Serotonin receptor subtype 5-HT2B, a G-protein-coupled receptor, play an important role in
serotonergic signaling. It is already known that its activation can modulate the 5-HT
concentration by its action on serotonin transporter. In addition, 5-HT2B knock-out mice show a
lack of antidepressants effect of SSRIs, an impulsive behavior, a loss ofMDMA psychoactive
effects. Allthosedrugsaretargetingtheserotonin transporter, it is why is crucial to know the
molecular mechanisms that are potentially disturbed in these processes. The 5-HT2B
receptorisstrongly associated to different kind of protein by its PDZ motif localized at the end of
its C-terminal extremity. Here we focused on channel interacting PDZ protein CIPP, a multivalent
PDZ domain protein know to form proteins complex and could act as an important
modulatorofglutamatergic transmission by its association to NMDA receptors. The present
study using transiently transfected cos-7 cell, show that interactions between 5-HT2B serotonergic
receptor and CIPP significantly increase signaling pathway activation in basal and stimulated
conditions without affecting G protein coupling efficiency to the receptor. Also,
pharmacological binding experiments indicates that association doesn’t affect the total and
plasma membrane expression of 5-HT2B receptor. Trafficking experiments using transiently
transfected primary culture of hippocampal neurons allowed us to identify CIPP clustering of 5-
HT2B receptors and modulation of its subcellular distribution.
Emilie SIMONNET, SabrinaMartin-Pires,LucPardanaud,AnneEichmann and Isabelle
Brunet - RoleofEphrine-A4 in the development and in the physiology of arterial
innervation
Molecular Control of Neurovascular Development - Collège de France
Arteries receive a sympathetic innervation which is crucial to control their contraction level.
Arterial innervation (AI) settles from post-natal day 2 (P2) to adult in mice. Gene expression
comparaison of non-innervated (P0) and innervated (P2) arteries showed that EphrinA4, a
repulsive axon guidance molecule, is surprisingly expressed by arteries at the onset of
innervation. Therefore we aimed to assess the role of EphrinA4 signalisation in the development
and the physiology of AI in mice. We showed by immunostaining and in situ hybridization that
EphrinA4 is expressed by resistance arteries and identified EPHA4 as the EphrinA4 receptor
expressed by sympathetic neurons (SN). In vitro EphrinA4 binds to WT SN and induces their
collapse, but not on SN from EphA4-/- mice. As an anatomical consequence of a lack of axonal
repulsion, EphrinA4-/- and EphA4-/- mice exhibit an enhanced AI at P2 which remains in adult.
We inactivated specifically EPHA4 within SN using THCre-EphA4flox/flox mice and showed an
increased AI in ear skin and on oesophagus. As peripheric vascular resistance is involved in the
regulation of blood pressure (BP) we hypothetized that the defects in AI observed in our mice
could lead to hypertension. We are currently investigating this hypothesis using telemetry. We
also investigated AI of organs regulating BP using the 3DISCO technic to stain the whole heart
and kidney. Our preliminary results suggest that EphrinA4/EphA4 signalisation would be involved
in cardiac and renal SI, showing an increased and more spread innervation. In conclusion,
EphrinA4 is expressed by arterial smooth muscle cells and interacts with EphA4 to induce
collapse of SN in vitro. In vivo this can be associated with elimination of inapropriate or
outnumbered contacts between SN and arteries. As peripheric vascular resistance is involved in
the regulation of BP, understanding development and physiology of AI could help us to open
new therapeutic ways for hypertension.
Pathophysiology
Mathieu BUONAFINE, Dr B. Gravez, Dr E. Martinez Martinez, Pr F. Jaisser and Dr C.
Amador – Implication of the Neutrophil Gelatinase-Associated Lipocalin (NGAL) from
immune cells in aldosterone induced cardiovascular remodeling
INSERM - Unité 1138, Equipe 1 - Esc E, 1er étage (Paris, France)
Background: Inadequate activation of the Mineralocorticoid Receptor (MR) promotes
hypertension, inflammation and fibrosis. Neutrophil Gelatinase-Associated Lipocalin (NGAL), a
pro-inflammatory/fibrotic glycoprotein, is a direct target of the MR in cardiovascular cells, and is
increased in immune cells during inflammation. Recently, we demonstrated that NGAL is crucial
for the hypertensive and pro-fibrotic effects of the nephrectomy-aldosteronesalt (NAS)
challenge in mice. However, the specific cell types that modulate NGAL production during
aldosterone-dependent hypertension are still unknown. The aim of this study was to characterize
the implication of NGAL produced by immune cells in the pathophysiological effects of MR
activation by aldosterone.
Materials and methods: In vivo: Male C57Bl6 mice were submitted to 28 days of NAS challenge
(200μg/kg/d). Peripheral blood mononuclear cells (PBMC) were isolated, and CD4+, CD8+ T
cells, B cells, Dendritic cells (DCs) and Macrophages (Mø) were sorted from the animals’ spleen.
In vitro: DCs and Mø were cultured from WT and NGAL-KO mice and treated with aldosterone
(100nM) for 24h.
Results: In vivo: NAS mice presented high systolic blood pressure (123 mmHg vs. Sham 101±6
mmHg, p<0.05), and cardiac/renal hypertrophy. NGAL abundance was found higher in PBMCs,
DCs and Mø, and further increased in NAS mice. In vitro: MR activation by aldosterone in DCs
induced an upregulation of NGAL and cytokines involved in the adaptive immune response
(TGF-β1, IL-23). Interestingly, the absence of NGAL in DCs cultured from NGAL-KO mice
prevented this increase.
Conclusion: MR activation and subsequent NGAL induction in DCs could play a pivotal role in
the inflammation observed during aldo-dependent hypertension.
Olivier CLAUDE, Elisa YANIZ-GALENDE, Maguelonne ROUX, Claire PERRET, David-
Alexandre TREGOUET and Jean-Sébastien HULOT - Identification of selective adult
cardiac progenitor cells (CPCs) surface markers by proteogenomics approaches
UMRS1166 – UPMC/INSERM, 91Bvd de l’hôpital, 75013 PARIS.
The presence of adult stem cells within the myocardium has only been recently acknowledged.
Using a transgenic mouse model expressing the bgalactosidase under the control of the PW1
gene, a marker of adult stem cell in numerous tissues, we have been able to identify new
populations of CPCs that contribute to myocardial repair after infarction. PW1 is however a
nuclear factor thus prompting for the identification of novel cell surface markers.We aim to
describe the membranome of those CPCs and its modification after MI in order to characterize
the function of those cells and in order to facilitate future studies.CPCs were collected from PW1-
bGAL mice normal and ischemic (7 days post MI) hearts using FACS. We used filtered, aligned,
quality controlled RNA-seq output files from each CPC population and condition (normal vs.
ischemic hearts) and converted RNA sequences into predicted protein sequences
(~40000/condition). A bioinformatic pipeline has been implemented in a Galaxy server to make
lists of putative membrane proteins by predicting the presence of signal peptides targeting
proteins to the membrane (SignalP3.0, WoLFPSORT) and transmembrane domains (TMHMM2.0)
but without nuclear localization signal (NLStradamus, PredictNLS).By progressive filtering, we
generated a list of candidates expressed in CPCs’ membranes (~2000/condition). By comparing
these different sub-types of CPCs and conditions protein lists, we identified cell type-specific and
condition-insensitive cell surface markers (~100proteins). Several databases were then cross-
checked to discard false positive results and a homebrew script was designed to create a
specific peptide list including sequences and molecular weight for the ~70 selected proteins.
Using same cells collected from the FACS, we proceed to a membrane protein enrichment
using a biotin coupled reagent. Sample will then undergo common proteomic treatments
before an LC-MS run in which we seek the specific peptide list previously described.
Irma Karen LOPEZ CAYUQUEO, Régine Chambrey, Jacques Teulon, Francisco V.
Sepúlveda, Isabel Cornejo and L. Pablo Cid - Knockin of HA-tagged K+ channel Kir7.1
as a tool to determine its segmental and subcellular localisation in mouse kidney.
PARCC INSERM U970, Centro de Estudios Cientificos (CECs).
Kir7.1 is an inwardly rectifying K+ channel of the Kir superfamily encoded by the Kcnj13 gene. This
channel is present in epithelial tissues where it was found to colocalize with the Na+/K+ pump by
immunohistochemistry and it was thus suggested it could serve to recycle K+ taken up by the
pump. We generated a mouse lacking Kir7.1 by ablation of the Kcnj13 gene; the homozygous
mutant null mice die hours after birth and show cleft palate and moderate retardation in lung
development.
In order to study more precisely the localisation of the Kir7.1 channel in tissues, we created a
Kir7.1 HA-tagged knockin mouse by the CRISPR/Cas9 method. The HA epitope (YPYDVPDYA)
was inserted between residues 90 and 91 of the extracellular loop of Kir7.1 channel. Additionally
one glycine (G) was added at the N-terminus of the epitope in order to improve both the
mobility of the tag and antibody recognizing. The insertion did not alter the function of Kir7.1 as
demonstrated in electrophysiological experiments on the channel in a heterologous expression
system. Our results corroborate previous localisation of Kir7.1 in choroid plexus and retinal
pigment epithelium, where the channel is seen at the apical membrane of these epithelial cells.
In the kidney, Kir7.1 protein was found only in the papilla by immunoblot analyses of the HA tag
on lysates of cortex, outer medulla and inner medulla. This restricted localisation does not fit with
previous immunohistochemistry studies on guinea pig, rat and human kidneys, in which the use
antibodies against Kir7.1 showed expression of this channel in the basolateral membrane of
various tubular structures in both cortex and medulla. Until now there was no report on the
localisation of this channel in the mouse kidney. The Kir7.1 HA-tagged mouse therefore is a good
tool to decipher the role of this potassium channel in the renal papilla, where important
processes such as urine concentration take place.
Ahmad MASSARWEH1,2,4, Michaël Bosco3, Soria Iatmanen-Harbi1,2, Clarice Tessier1,2,
Nicolas Auberger3, Patricia Busca3, Isabelle Chantret1,2, Christine Gravier-Pelletier3 and
Stuart E. H. Moore1,2 - Golgi Dolichol linked Oligosaccharide (DLO) Diphosphatase, a
potential regulator of DLO metabolism 1INSERM U1149, Paris, France. 2Université Denis Diderot, Paris 7, Paris, France. 3Université Paris Descartes, CICB-Paris, CNRS UMR8601, LCBPT, 45 rue des Saints-Pères, 75006 Paris, France. 4Université Pierre et Marie Curie, Paris 6, Paris, France.
Background: Type I congenital disorders of glycosylation (CDG-I) are caused by genetic defects
in the Dolichol-Linked Oligosaccharide (DLO) biosynthetic pathway. These mutations result in the
accumulation of DLO intermediates and protein hypoglycosylation. Although protein
hypoglycosylation is thought to be the main pathogenic factor in CDG-I, the pathogenic effect
and fate of truncated DLO intermediates is not understood. Truncated DLO intermediates in
patient’s cells are known to give rise to cytosolic Oligosaccharyl Phosphates (OSP) by an
uncharacterized mechanism. To understand this DLO editing process; characterization of the
activity that generate OSP at the molecular and biochemical levels is needed.
Materials, methods and results: Using classical biochemical approaches we characterized a
Co2+ activated DLO diphosphatase which has a pH optimum 5.5 and generates OSP and
dolichyl phosphate from DLOs. Differential centrifugation of mouse liver showed a microsomal
localization of this activity. Fractionation of microsomes on self-forming density gradient
demonstrated that the activity doesn’t co-localize with the Endoplasmic Reticulum (ER)-situated
dolichol cycle enzymes (where DLOs are synthesized and utilized) but with the Golgi Apparatus
(GA)-situated marker (UGT). The unexpected localization profile prompted us to study OSP
generation in cells using Brefeldin A (BFA) which fuses elements of GA with ER. BFA caused a
striking increase in OSPs that have Golgi modified structures. Further OSP localization studies
using permeabilized cells revealed that BFA induced OSP generation in the lumen of the BFA
compartment contrary to cytosolic OSPs generated in CDG-I cells which was not affected by
BFA treatment.
Conclusion: OSP generation is a complex process governed by at least two mechanisms
depending on DLO structure, membrane orientation and localization. We propose that the GA
situated DLO diphosphatase may play a role in degrading the DLO that escape the ER.
Meriam NEFLA, Laure SUDRE, Guillaume DENAT,Sabrina Priam, Gwenaëlle Andre-Leroux,
Francis BERENBAUM and Claire JACQUES - The proinflammatory cytokine 14-3-3ε is a
ligand of CD13 in cartilage.
CDR Saint-Antoine UMR_S 938, 184 Rue du Faubourg Saint-Antoine, 75012 Paris
Background: Osteoarthritis (OA) is a whole-joint disease characterized by progressive destruction
of articular cartilage involving abnormal communication between subchondral bone and
cartilage. Our team identified 14-3-3ε protein as a subchondral bone soluble mediator altering
cartilage homeostasis. This protein acts as a potent stimulatory factor of MMP-3 and MMP-13
involved in the degradation of cartilage matrix in OA. CD13/APN, potential receptor of this
protein, was identified on the surface of chondrocytes. The aim of this study was to investigate its
involvement in chondrocytes response to 14-3-3ε.
Methods: CD13/APN was invalidated using siRNA or blocking antibodies in articular
chondrocytes. Chondrocyte expression and release of MMP-3 and MMP-13 were evaluated by
RT-PCR and ELISA. The aminopeptidase N (APN) activity was assessed in chondrocytes
supernatant using the fluorescent substrate L-alanine β-naphtilamide. The interaction between
14-3-3ε and CD13 was studied by surface plasmon resonance, biotinylation and in silico studies.
Results: mRNA expression and protein release of MMP-3/-13 induced by 14-3-3ε reduce
significantly after CD13/APN invalidation. APN activity was identified in chondrocytes. However,
it was unchanged following chondrocyte stimulation with 14-3-3ε. Direct interaction was showed
between recombinant CD13/APN and 14-3-3ε (78 RU). Using labeled 14-3-3ε, we also found that
14-3-3ε binds to the surface of chondrocytes in a CD13 dependant manner . Finally, we
identified EFNpYVW as the CD13 peptide sequence required for the recognition of 14-3-3ε.
Conclusions: These results suggest that CD13 plays its receptor role to bind 14-3-3ε and transmit
its signal in chondrocytes to induce a catabolic phenotype similar to that observed in OA. Thus,
14-3-3ε-CD13 interaction could be a novel therapeutic target in OA.
Benjamin VALLIN, Régis Blaise, Isabelle Limon - Identification of a new adenylyl cyclase
8 (AC8) isoform: implication in vascular smooth muscle cells (VSMCs)
transdifferentiation and pathological vascular remodeling
UMR 8256 Biological Adaptation and Ageing
Atherosclerotic lesion expansion and post-angioplasty restenosis result primarily from the
transdifferentiation of VSMCs into migratory/proliferative/inflammatory/secretory cells. Cyclic
AMP, whose production and degradation are catalyzed by adenylyl cyclases (AC) and
phosphodiesterases (PDE) respectively, plays a key role in modulating VSMCs phenotype
(Yokoyama, 2010).
We showed that the transdifferentiation of VSMCs into inflammatory/migratory cells in vitro
depends on de novo expression of the transmembrane AC isoform 8. The pathological VSMCs in
human atherosclerotic lesions have high AC8 levels. AC8 knockout in ApoE-/- mice decreased
aorta inflammation and lesion size; the siRNA-mediated knockdown of AC8 reduced neo-intima
formation in a rat model of postangioplasty restenosis.
We recently discovered that 90% of the AC8 in transdifferentiated (td) VSMCs consists of a newly
identified splice variant lacking the first five transmembrane domains: AC8D.
Immunocytochemistry and AC activity assays revealed a profound change in membrane
topology knocking AC8D activity. Surprisingly, studies with FRET-based biosensors showed that
AC8D limits cAMP accumulation within the cell. Studying cAMP synthesis over time, we showed
that AC8D has no effect on cellular AC activity. Thus, the inhibition of cAMP accumulation results
from an increase in PDE activity, suggesting a role for AC8D in physically recruiting PDE, by direct
activation or subcellular relocalization. Furthermore, using AC8D-specific siRNA, we
demonstrated the involvement of AC8D in the transdifferentiation of VSMCs into inflammatory
cells.
Increases in cellular cAMP inhibit the migratory (McKean, 2015), proliferative (Hewer, 2011) and
inflammatory (Aoki, 2010) properties of tdVSMCs. Thus, AC8D may participate in atherogenesis
and restenosis by maintaining the pathological phenotype of tdVSMCs. We are investigating the
mechanisms involved and trying to confirm the role of AC8D in pathological vessel remodeling.
ORAL COMMUNICATIONS - 26th May 2016
Immunology & Inflammation
Mélanie CRON, Frédérique Truffault, Ambra Vittoria Gualeni*, Annunziata Gloghini*,
Sonia Berrih-Aknin and Rozen Le Panse - Characterization of the role of miR-150 in
autoimmune Myasthenia Gravis
UPMC - UMRS 974 - INSERM - FRE 3617 CNRS - AIM Centre de Recherche en Myologie - Hôpital de La Pitie-
Salpétrière
*Department of Pathology and Laboratory Medicine, Istituto Nazionale dei Tumori, Milano, Italy
Myasthenia gravis (MG) is an invalidating disease mediated by autoantibodies against the
acetylcholine receptor at the neuromuscular junction and leading to muscle weaknesses. In
MG, the thymus is the effector organ and is often characterized by B-cell infiltrations leading to
ectopic germinal center (GC) development. MicroRNAs are small noncoding RNAs that regulate
protein expression through direct interactions with mRNAs. They are involved in many
physiological and pathophysiological processes, including autoimmune diseases. In
collaboration with a Swedish team, we demonstrated that miR-150 was upregulated in the
serum of MG patients, and was significantly downregulated after thymectomy in correlation with
disease improvement.
The aim of this study was to determine the potential role of miR-150 in MG patients by
investigating its expression in the thymus.
We showed that miR-150 was upregulated in the thymus of MG patients with numerous GCs. We
did not observe any miR-150 increase in thymic epithelial cells or in thymocytes from MG patients
compared to controls. However, miR-150 increase was correlated with thymic expression of the
B-cell marker CD19. By in situ hybridization, we demonstrated that miR-150 was strongly
expressed in naive B cells located in the mantle zone around GCs.
We also observed that thymic expression of c-Myb, a well-defined target of miR-150, was down-
regulated and inversely correlated with the expression of miR-150. In naïve B cells of the mantle
zone, miR-150 expression is probably involved in the regulation of c-Myb at a posttranscriptional
level, blocking B-cell differentiation.
Altogether, we demonstrated that the thymic up-regulation of miR-150 in MG is correlated with
the abnormal development of GCs in patients. We are now investigating why miR-150 is
increased in the serum of MG patients and if this circulating miR-150 has a functional role in the
disease.
Clément LEVIN1,2*, Charles Nuttens1,2*, Olivia Bonduelle1,2, Helene Perrin1,2, Bernard
Verrier3 and Béhazine Combadiere1,2 - Role of skin migratory antigen-presenting cells in
T follicular helper cell polarization after intradermal vaccination
*Both authors contributed equally to this work 1Sorbonne Universités, UPMC Univ Paris 06, Unité Mixte de Recherche de Santé (UMR S) CR7, Centre
d’Immunologie et de Maladies Infectieuses – Paris (Cimi-Paris), F-75013, Paris, France 2Institut National de Santé et de Recherche Médicale (INSERM) U1135, Cimi-Paris, F-75013, Paris, France 3Institut de Biologie et Chimie des Protéines, Centre National de la Recherche Scientifique, Université
Claude Bernard de Lyon, 69367 Lyon
Cedex 07, France
Background: The skin is recognized as a promising route of immunization as it contains
specialized APC subsets such as Langerhans cells (LCs) and other dermal dendritic cells (DCs).
Upon immunization, DCs in tissues sample antigens and migrate to draining lymph nodes (DLNs)
where they interact with naïve T cells to promote their differentiation and effector functions. In a
previous work we showed that intradermal (i.d) immunization of mice with HIV-p24 poly lactic
acid (PLA) nanoparticles induced robust humoral and cellular CD8+ T cells responses, which are
crucial against HIV disease.
As T follicular helper (TFH) cells play a pivotal role in germinal center formation and B cell help,
we questioned the role of skin and DLN APCs in the induction of TFH cells and antibody-secreting
B cells after i.d vaccination.
Methods: Ablation of the injection site and conditional depletion of langerin+ cells were used to
evaluate the role of skin migratory cells and langerin-expressing cells respectively in TFH cell
induction. Moreover, fluorescent antigen-coated nanoparticules (NPs) were used as a vaccine
model to enable tracking of NPs+ cells.
Results: We found that skin migratory DCs are necessary for induction of TFH and antigen-specific
antibody-secreting B cells. Tracking of injected p24-PLA NPs revealed the high ability of LCs and
Langerin+ dermal DCs to capture antigen in the skin and migrate to the T/B interface of DLNs.
Further depletion of Langerin+ cells resulted in partial abortion of TFH polarization and p24-
specific IgG and IgA-secreting B cells expansion after immunization.
Conclusions: Work is currently in progress to elucidate the mechanisms by which skin mig DCs
promote such responses after i.d vaccination. Our work unravels a crucial role for skin cells and
particularly LCs in the induction of humoral immunes responses and TFH cell polarization after i.d
vaccination. It will provide cues for better vaccine development against infectious diseases such
as HIV.
Anastasia MIKHAILOVA1, Robbiati V2, Lasserre R2, Pinaud L2,3, Alcover A2, Rey F1 and
Thoulouze MI1,2 - The role of Tuba protein in the dynamics of immune synapse formation 1Structural Virology Unit, Department of Virology, Institut Pasteur, Paris, France 2Lymphocyte Cell Biology Unit, Department of Immunology, Institut Pasteur, Paris, France 3Molecular Microbial Pathogenesis, Department of Cell Biology and Infection, Institut Pasteur, Paris, France
T lymphocytes commonly make contacts between each other and antigen presenting cells
(APCs). The formation and signal propagation in activating contacts, termed immunological
synapses (IS), strongly depend on the reorganization of the cell’s cytoskeleton and intracellular
trafficking. However, the exact molecular players responsible for these events still remain poorly
understood.
Tuba is a multidomain scaffolding protein that has a lipid-binding BAR domain and interacts with
N-WASP and Cdc42, molecules coordinating cell polarization at the IS. Upon Tuba knockdown
(KD), T cells displayed reduced ability to retract from contacts with a glass surface but formed
less stable and symmetric IS with APCs. Moreover, T cell receptor (TCR) displayed fragmented
accumulation pattern at the IS, which was accompanied by increased cell activation, reflected
by higher IL-2 production. However, the identity of the intracellular events connecting the
change in the nature of contacts with increased T cell activation still needs to be determined.
We performed live cell imaging to directly observe real time dynamics of IS formation in Tuba KD
and control cells. When dropped on glass coated with activating anti-TCR antibody, T cells
transfected with C-terminal domain of Tuba (mimics KD) displayed higher asymmetry at the
contact interphase but there was no observable difference in the speed of TCR signaling
microclusters. Although no differences were observed in calcium signaling in Tuba KD cells and
controls during contacts (both activating and non-activating) with B cells, Tuba KD cells
displayed slower migration speed and less displacement during the interaction with dendritic
cells confirming retarded retraction pattern seen on glass.
We conclude that there are no differences between Tuba KD and control cells in the early
events of the cell signaling downstream of the TCR. Thus, the increase in activation is due to
changes in the late phase of the T cell contact dynamics.
Emmanuel STEPHEN-VICTOR1,2,3, Srini V Kaveri1,2,3,5, Jean-Paul Latgé4, Vishukumar
Aimanianda4 and Jagadeesh Bayry1,2,3,5 - Cellwallα-(1,3)-glucanfrom Aspergillus
fumigatus induces PD-L1 expression on human dendritic cells that regulates Th1 and
regulatory T cell responses 1Institut National de la Santé et de la Recherche Médicale Unité 1138, Paris, F-75006, France 2Sorbonne Universités, UPMC Univ Paris 06, UMR S 1138, Paris, F-75006, France 3Centre de Recherche des Cordeliers, Equipe - Immunopathology and therapeutic immunointervention,
Paris, F-75006, France 4Unité des Aspergillus, Institut Pasteur, Paris, F-75015, France 5Université Paris Descartes, Sorbonne Paris Cité, UMR S 1138, Paris, F- 75006, France
Background: Aspergillus fumigatus is an opportunistic pathogen that causes invasive
aspergillosis, a fatal disease in immune-compromised individuals. Cell wall polysaccharides are
the key immunogenic components of A. fumigatus. α-(1,3)-glucan, an amorphous component
of A. fumigatus cell wall forms a major proportion among cell wall polysaccharides suggesting
that this polysaccharide has a critical role in modulating immune response. In the present study
we investigated the role of A. fumigatus derived α-(1,3)-glucan in mediating human DC
response and the ensuing T cell response.
Materials and Methods: Human dendritic cells (DCs) were derived from circulating monocytes.
DCs were treated with α-(1,3)-glucan and the extent of DC maturation and activation was
analyzed by flow cytometry. The ‘α-(1,3)-glucan-educated’ DCs were co-cultured with
autologous naïve CD4+ T cells to delineate the polarization of T cell responses by flow cytometry.
Cytokine production by DCs and T cells was analyzed by ELISA.
Results: α-(1,3)-glucan induced maturation of DCs and secretion of various immunoregulatory
cytokines. Of note, activation of innate cells was partially dependent on TLR2. Analysis of CD4+ T
cell polarization revealed that α-(1,3)-glucan-stimulated DCs induced CD4+ CD25+FoxP3+
regulatory T cell (Treg) generation that was in part dependent on programmed death-ligand 1
(PD-L1) expression on DCs. Importantly, blockade of PD-L1 on DCs enhanced IFN-γ secretion
suggesting that PD-L1 acts as negative regulator of α-(1,3)-glucan-mediated protective immune
responses. Taken together, these results demonstrate that α-(1,3)-glucan diversifies the immune
response to A. fumigatus by their distinct abilities to polarize specific CD4+ T cell responses.
Conclusion: A. fumigatus derived α-(1,3)-glucan is an immunomodulatory polysaccharide that
imprints regulatory features on DCs which suppresses Th1 response and mediates Treg
generation.
Virology
Iratxe DEL RIO, Jérôme Bouchet, Andrés Alcover - HIV-1 modulation of the T cell
activation molecular machinery
Lymphocyte Cell Biology, Inserm U1221, Institut Pasteur, Paris
The actin and microtubule cytoskeleton, together with polarized vesicle traffic, play a major role
in the formation and function of immunological synapses, ensuring the spatiotemporal
localization of the T cell receptor (TCR) and different signaling proteins. Our laboratory showed
that HIV-1 subverts the formation of immunological synapses. Indeed, HIV-1, through its protein
Nef, interrupts the intracellular transport of the tyrosine kinase Lck, a key element of the TCR
signal transduction cascade, to the immunological synapse, inducing its accumulation in an
intracellular vesicular compartment.
We utilized wild type or Nef-deficient HIV-1 virus strains, expression vectors encoding Nef or
various cellular proteins, and state of the art microscopy techniques to characterize this Nef-
induced endosomal compartment. Experiments performed both with Nef-expression or HIV-1
infection of the Jurkat T cell line show that Nef recruits active (phosphorylated) forms of several
key TCR signaling molecules, like the TCRz subunit, the tyrosine kinase ZAP70 and Vav1 to the Lck
compartment, where they strongly colocalize with Lck. Nef also recruits Rac1, an important
GTPase involved in actin remodeling, in a compartment, different that the one of Lck, where
Rac1 and Nef fully co-localize. Importantly, we showed the interaction between Nef and Rac1
by co-immunopecipitation experiments. Therefore, Nef could modulate, through this interaction,
the actin cytoskeleton dynamics.
We also observed that FIP3, a Rab11 effector protein, participates in this Nef-induced Lck
accumulation in endosomes, as FIP3 silencing by siRNA, disassembles the Lck compartment and
counteracts the effect of Nef on Lck endosomal accumulation. As a result, FIP3 silencing
provides an opportunity to perturb the Nef-induced endosomal compartment to investigate its
relevance in the physiology of infected T lymphocytes in order to modulate their activation
state, their survival capacity and to improve viral replication.
Olivier LUCAR1, 2, Bin Su3, Valérie Potard4, Assia Samri1, Christiane Moog3, Patrice Debré1,
Vincent Vieillard1 and ANRS CO15 ALT study group - New Family of Neutralizing
Antibodies in HIV Asymptomatic Long-Term Non-Progressors 1Sorbonne Universités, UPMC Univ Paris 06, INSERM U1135, CNRS ERL8255, Centre d’Immunologie et des
Maladies Infectieuses (CIMI-Paris), Paris, France; 2InnaVirVax SA, Evry, France, 3INSERM UMR S-1109, Centre de Recherche en Immunologie et Hématologie, Faculté de Médecine,
Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Strasbourg,
France; 4Sorbonne Universités, UPMC Univ Paris 06, INSERM UMR-S 1136, Institut Pierre Louis d'Epidémiologie et de
Santé Publique, Paris, France
One of the most debated issues in HIV is: do Neutralizing Antibodies (NAbs) plays a protective
role during HIV infection?
Through a large series of studies, our team previously characterized the pathogenic effect of the
highly conserved 3S epitope of gp41 during HIV infection. By analyzing the immune response
induced in asymptomatic long-term non-progressor (ALT) patients, we recently observed that
25% patients elicited efficient neutralizing responses directed against a point-mutated form of 3S
(W614A-3S). Thus, we extensively characterized the neutralizing profile of this new family of Nabs.
Abs binding to 3S-WT (wild-type) or W614A-3S mutants were isolated from the sera of ALT
patients. Abs were purified from heat-inactivated plasma of ALT patients by
immunoprecipitation with synthetic W614A-3S peptides immobilized onto an amine-reactive
agarose support, concentrated with Centicon filter, and dialyzed against PBS. The functional
inhibitory profile of these Abs was defined using the well-standardized TZM-bl neutralization
assay, the neutralization assay on PBMCs, or the Fc-mediated inhibitory assay on macrophages.
We found that the anti-W614A-3S purified Abs display efficient and broad neutralizing activity.
They inhibit transmitted founder Tier 2 viruses, neutralize primary isolates on primary cells and
display Fc-mediated inhibitory functions at low concentrations. The detection of anti-W614A-3S
Abs was specifically correlated both with lower viral DNA (p<0.0001), viral load (p<0.0001), and
more functional CD4+ cells; suggesting that anti-W614A-3S neutralizing Abs participate in the
control of HIV replication.
These results demonstrate ALT patients develop efficient neutralizing Abs distinct of those
recently isolated from ELITE neutralizer patients. Abs directed against W614A-3S may therefore
be considered as a new family of broadly neutralizing Abs, which need to be further
characterized, considering their potential role on viral load and viral DNA.
Angeline ROUERS, Brunet H., Moris A., Graff-Dubois S. and collaborators - Follicular
helperT cells (Tfh) and memory B cell response during HIV-1 infection Center for Immunology and Microbial Infections (CIMI-Paris), INSERM U1135, CNRS ERL8255, UPMC UMRS
CR7 - Hôpital Pitie-Salpêtière – France
T follicular helper cells (Tfh) support multiple steps of B cell maturation and antibody production.
HIV infection is associated with a defect of Tfh in providing B cell help in vitro. Mechanisms
underlying these Tfh dysfunctions are not fully defined. However, few HIV-infected individuals
known as elite controllers (EC) are able to produce polyfunctional antibodies (Ab), which might
contribute to HIV control. We first studied Tfh cells in chronically HIV-infected patients and in a
second complementary approach, we explored B cell memory responses in EC.
We identified Tfh, germinal center Tfh and regulatory Tfh in HIV+ and HIV spleens by FACS. These
three populations were increased in HIV+ spleen as compared to HIV- spleens. Using cell sorting
combined with RT-qPCR, we reported a reduced mRNA expression of co-stimulatory, regulatory
and signal transduction molecules in HIV+ spleens. We also evidenced compromised
productions of IL-4 and IL-10 by splenocytes from HIV+ donors. In parallel, we noticed an
impaired maturation of B cells in HIV+ spleens.
In a cohort study, we compared memory B cell responses in the blood of EC, treated HIV+
patients and healthy controls. Based on CD27 and CD21 expression, we identified activated,
resting, tissue-like and intermediate memory B cell by FACS. Our preliminary analysis suggests
that a HLAB* 57neg subgroup of EC presents an altered differentiation of B cells as compared to
others. Using B cell Elispot assays, we determined frequency, IgG isotype and specificity of anti-
HIV memory B cells. In contrast to anti-HIV IgG2 and IgG3 secreting B cells, most EC exhibit a high
frequency of anti-HIV IgG1 secreting B cells.
My work highlights a defective Tfh differentiation, which might explain why B cell maturation is
severely affected in HIV-progressors. The status of HIV-controllers seems associated with the
presence of an IgG1 B cell memory response. Further work will highlight whether Tfh functions are
preserved in EC.
Zineb SBIHI1, Dossier A1,4, Galicier L3, Boutboul D3, Emarre A1, Parizot C1,2, B Hoareau5,
Abgalika F3, Autran B1,2, Oksenhendler E3 and Carcelain G1,2 - iNKT and Memory B cells
deficiency in HHV-8 Multicentric Castleman Disease. 1Sorbonne Universités, UPMC Univ Paris 06, Inserm, Centre d'Immunologie et des Maladies Infectieuses
(Cimi-Paris), UMR 1135, ERL CNRS 8255, 91 Boulevard de l'Hôpital, F-75013 Paris, France 2Sorbonne Universités, UPMC Univ Paris 06, Inserm, Centre d'Immunologie et des Maladies Infectieuses
(Cimi-Paris), UMR 1135, ERL CNRS 8255, 91 Boulevard de l'Hôpital, F-75013 Paris, Département
d’Immunologie, CHU Pitie-Salpêtrière, Assistance Publique-Hôpitaux de Paris, 47-83 bd de l'hôpital, F-75013
Paris, France 3Hôpital Saint-Louis, Immunologie clinique, F-75010 Paris, France 4Hôpital Bichat, Médecine Interne, F-75018 Paris, France 5Sorbonne Universités, UPMC Univ Paris 06, UMS30-LUMIC, Platerforme CyPS, Paris, France.
Human Herpes Virus-8 (HHV-8) related Multicentric Castleman Disease (HHV-8 MCD) is a
lifethreatening virally induced B cell lymphoproliferative disorder. CD1d-restricted invariant
Natural Killer T (iNKT) cells, are innatelike T cells, playing a key role in antiviral immunity in
particular in the control of Epstein Barr Virus (EBV) infected B cells. We analyzed iNKT cells in
blood and spleen samples from 32 HHV-8 MCD patients and showed that iNKT cell frequencies
were dramatically decreased. Moreover, iNKT cells of HHV-8 MCD patients displayed a
significant proliferative defect after stimulation with α-GalCer. This defective iNKT cell was
associated with altered B cell subsets distribution, with a significant decrease in memory B cells
far more pronounced in Marginal Zone B cells. However, we observed no defect in CD1d
expression in antigen presenting cells but we showed that the iNKT defects contribute to the B
cell subsets alteration. This study identifies for the first time a defect in iNKT cell in HHV-8 MCD
patients associated to an imbalance in B cell subsets. These observations may contribute to the
understanding of the complexe interaction between HHV-8 and immune system cells leading to
the development of HHV-8 related B cell malignancies in HHV-8 MCD patients.
Metabolism & Nutrition
Mengyue HU Franck PHAN, Isabelle HAINAULT, Fawaz ALZAID, Nicolas VENTECLEF, Olivier
BOURRON, Fabienne FOUFELLE - The role of receptor activator of NF-kB (RANK) and its
ligand (RANKL) in the Non-Alcoholic Fatty Liver Disease (NAFLD)
INSERM UMRS 1138, Centre de Recherches des Cordeliers, 75006 Paris, France
Background and aim: Chronic inflammation in liver plays an important role in the development
of non-alcoholic fatty liver disease (NAFLD), a metabolic syndrome that encompasses a
spectrum of diseases. The activation of Nuclear factor-kB (NF-kB) in liver contributes to steatosis,
insulin resistance, hepatic inflammation leading to hepatic fibrosis. Among the numerous system
that activates NF-kB, RANKL and its cognate receptor RANK have been recently reported to be
involved in the progression of insulin resistance and other metabolic diseases. The aim of the
project is to study the RANK/RANKL/NF-kB pathway in the onset and progression of NAFLD.
Methods: The expression of RANK and RANKL under different pathological conditions related to
NAFLD were measured in different cells of the liver (hepatocytes, Kupffer cells, and Hepatic
Stellate cells) and adipose tissue. To activate the RANK/RANKL pathway in vivo, recombinant
RANKL was injected for 4 consecutive days in wild type mice.
Results: Under NAFLD conditions, the expression of RANK and RANKL was induced in
hepatocytes, kupffer cells, and hepatic stellate cells, and the increase was more remarkable as
the inflammatory states aggravated. RANK and RANKL expression were also induced in the
adipose tissue of ob/ob mice, and adipocytes of diabetic patients.
After repeated injections of RANKL, no obvious alterations were observed in liver, but in
epididymal adipose tissue, numerous lipogenesis genes were induced, along with the induction
of proinflammatory cytokines. Similar increase of lipogenesis genes was also observed in
subcutaneous adipose tissue.
Conclusion: The expression of RANK and RANKL are increased in liver and adipose tissue under
conditions related to NAFLD. The activation of RANK/RANKL pathway could play a role in the
lipid metabolism of adipose tissue.
Cécilia LANDMAN, M. Clément, H. Nsiri, E. Quévrain, T. Bazin, L. Brot, J.-P. Grill, M.-A.
Maubert, L. Humbert, H. Sokol, G. Trugnan, D. Rainteau and P. Seksik – The N-acyl-
homoserine lactone 3-oxo-C12, an inter-bacterial signaling molecule (involved in
quorum sensing), exerts effects on the host: thus implicating quorum sensing in
Inflammatory Bowel Disease
UPMC, ERL INSERM 1157 / UMR7203, Paris, France
Background: Inflammatory bowel disease (IBD) associated dysbiosis causes profound changes in
gut microbiota. We have shown previously that the profile of inter-bacterial signaling molecules,
the N-acyl-homoserine lactones (AHLs), is altered during dysbiosis. In particular, we observed
deficiency in 3-oxo-C12:2, the dominant intestinal ecosystem AHL. The aim of this study was to
explore the ability of 3-oxo-C12, a structurally close AHL, to interact with eukaryotic intestinal
epithelial cells.
Methods: Firstly, the subcellular localization of fluorescently labeled 3-oxo-C12 was visualized, in
a human epithelial cell (Caco-2) model, by confocal microscopy. Additional staining included:
membranes stained with Lectin Wheat Germ agglutinin (WGA), nucleus with DRAQ 5 and
euchromatin with anti-histone3 antibody. Following this, we examined the effect of 3-oxo-C12 on
inflammation pathways. Experiments were carried out under a range of conditions including:
increasing concentrations in DMSO, with/without the paraoxanase (PON) inhibitor, 2-
hydroxyquinoline (2HQ) and with/without IL1β stimulation. Response was quantified by
measurement of IL-8 (ELISA) in the supernatant 18 hours post exposure to AHL.
Results: Confocal microscopy showed intracellular localization of 3-oxo-C12 (1μM) after 1 hour.
More specifically, we observed co-localisation with euchromatin suggesting a transcriptional
factor role for 3-oxo-C12 within the host cell.
When examining the effect of 3-oxo-C12 on inflammation pathways we observed a significant
decrease in IL-8 18 hours post stimulation with IL1β, in the presence of both 3-oxo-C12 (1 and
5μM) and 2HQ.
Conclusion: We have demonstrated that 3-oxo-C12, an AHL structurally close to 3-oxo-C12:2,
present in the human intestinal ecosystem interacts with eukaryotic cells by penetration of
intestinal epithelial cells. Additionally, 3-oxo-C12 exerts an anti-inflammatory effect, at low
concentrations, in the presence of PON inhibitors in the same cell model.
Ludovica MARINELLI1, Camille Martin-Gallausiaux1, Fabienne Beguet-Crespel1, Karine
Clément2, Hervé M. Blottiere1,3, Nicolas Lapaque1 - Activation of the AhR signal pathway
by the gut microbiota. 1Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, Jouy-en-Josas, France; 2Institute of Cardiometabolism and Nutrition, ICAN, Assistance Publique Hôpitaux deParis, Pitie-Salpêtrière
hospital, Paris ; 3MGP MetaGenoPolis, INRA, Université Paris-Saclay, Jouy en Josas, France.
Microbiota shapes the host metabolic and immune network producing metabolites acting as
physiological or immunological modulators. Within these bacterial products, indoles have been
described as AhR ligand inducing anti-inflammatory response. However, the interplay between
host and microbiota is highly complex and the precise mechanism for microbial AhR stimulation
is still unclear. We aim to identify: i) the bacteria able to activate AhR, ii) the genes involved, iii)
the produced molecules and iv) the potential effect for the host. For this purpose, we screened
a collection of bacterial species on HT-29 cell line expressing an AhR luciferase reporter system
and we identified 32 AhR-activators and 15 AhR-inhibitors strains. Principal component analysis
evidenced a correlation between AhR activation and butyrate production that we confirmed
with pure butyrate. Test of other SCFA evidenced also a reproductive AhR activation by
propionate, isovalerate and valerate. To identify the mechanism by which butyrate activates
AhR, we tested the impact of agonists of G-protein coupled receptors (GPR) and inhibitors of
histone deacetylase (HDACi) on AhR activation. GPR agonists as well as HDACi did not mimic
the effects of butyrate, suggesting a mechanism independent of both GPR and HDAC. We test
therefore two AhR antagonists and we showed that both failed to completely suppress the
butyrate-induced response suggesting two different hypotheses: i) butyrate is not an AhR ligand;
ii) butyrate is an AhR ligand with mechanism of activation or affinity different from the known
ligands. We are currently studying the mechanism by which butyrate activates AhR, by
analysing the expression of some crucial partners of the AhR activation pathway. Interestingly
we also identified bacterial strains able to activate AhR without butyrate and propionate
production and these will be used to generate genomic libraries for the identification of the
bacterial metabolites and genes involved.
Hedi SOUSSI, Sophie Reggio, Rohia Allili, Cecilia Prado, Maria Pini, Christine Rouault,
Karine Clément and Isabelle Dugail - DAPK2 down-regulation associates with
attenuated adipocyte autophagic clearance in human obesity
INSERM U1166 – Nutrition and obesity – Systemic approaches University Pierre and Marie Curie, Paris, France
Obesity is defined by excessive accumulation of fat and represents a condition wherein the
proper sensing of nutrients and energy status present significant challenges at the cellular and
systemic levels. The subsequent emergence of metabolic alterations and oxidative stress lead to
inflammation and organelle dysfunction. In this context, the autophagy pathway, which
orchestrates the degradation of damaged cytosolic constituents, is expected to be a critical
process for metabolic adaptation and cellular homeostasis. We analyzed autophagic flux in
adipocytes from obese patients (undergoing bariatric surgery) and obese mice. Adenoviral
approaches were used in adipocyte cell line to modulate autophagy-related protein
expression.
We observed a downregulation of autophagy in adipocytes from obese patients and obese
mice. Moreover, the degree of fat cell hypertrophy is inversely associated to autophagy activity,
suggesting a link with lipid storage. Our transcriptomic analysis of obese adipose tissue showed a
strong downregulation of the gene coding death associated protein kinase 2 (DAPK2).
Interestingly, suppression of DAPK2 in vitro resulted in defective autophagy, whereas
overexpression of this kinase increased autophagy in adipocyte cell line. Finally we observed a
partial restoration of autophagic activity and DAPK2 expression in adipocyte after weight loss
induced by bariatric surgery.
These data showed a link between DAPK2 downregulation and defective autophagy in obesity
and suggest an involvement of this kinase in adipocyte dysfunction.
POSTERS
Wednesday, 25th May 2016 – 10:30 to 11:45
[1] ANDROUIN Alexandre, Youssef, I., Delatour, B. and Marty, S. - Endoplasmic reticulum stress
and neurodegeneration in a mouse model of Alzheimer's Disease
Team "Alzheimer's and Prions's diseases", Brain and Spinal cord Institute, Inserm U1127/CNRS UMR
7225/UPMC Univ Paris 06 UMR S 1127, Paris, France
[2] BEGUIER Fanny, Michael Housset, Sophie Lavalette, Sébastien Augustin, Xavier Guillonneau
and Florian Sennlaub - HTRA1 and subretinal inflammation in the context of Age Macular
Degeneration
Institut de la Vision U968
[3] BENABOU Eva, Corina Buta, Dominique Wendum, Olivier Scatton, Olivier Rosmorduc,
Françoise Praz, Laëtitia Fartoux and Christèle Desbois-Mouthon - Insulin receptor isoform A in
hepatocellular carcinoma
CdR Saint Antoine, UMR_S938
[4] BOTTE Alexandra, Jeanne Lainé (1), Gaëlle Fontaine (1), Agathe Franck (1), Dean Nizetic (2),
Orestis Faklaris (3) and Marie-Claude Potier (1) - Early endosomes agregation in Down Syndrome
and Alzheimer's disease (1) Institut du Cerveau et de la Moelle épinière, Paris
(2) Barts and London School of Medicine, Queen Mary University, London
(3) Plateforme ImagoSeine, Institut Jacques Monod, Paris
[5] BOUGACHA Nadia - Role of REL in drug resistance in Chronic Lymphocytic Leukemia
Centre de Recherche des Cordeliers UMRS 1138
[6] BOUVET Delphine (1,2), MUNIER Annie (3), SVRCEK Magali (1,2,4), DUVAL Alex (1,2) and
MULERIS Martine (1,2) - Diagnosis of Lynch syndrome: functional characterization of variants of
uncertain significance in mismatch repair genes
(1) INSERM UMRS 938 -Centre de Recherche Saint-Antoine, Equipe "Instabilité des Microsatellites et
Cancers", Paris, France
(2) Université Pierre et Marie Curie-Paris6, Paris, France
(3) UMS30-LUMIC, Plateforme de Cytométrie en Flux CISA, Université Pierre et Marie Curie, Paris, France
(4) AP-HP, Hôpital Saint-Antoine, Service d'Anatomie et Cytologie Pathologiques, Paris, France.
[7] BOUYGUES Anaïs, Paul Mésange, Sandrine Thouroude, and Annette K. Larsen - VEGF-directed
therapies directly attenuate the migration and invasion of colorectal cancer cells
Laboratory of Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris 75571, France;
Institut National de la Santé et de la Recherche Médicale U938, Paris, France; Université Pierre et Marie
Curie, Paris France.
[8] COHEN Romain (1), Elisabeth Hain (1), Olivier Buhard (1), Sylvie Dumont (1), Thierry André (1,
2), Magali Svrcek (1, 3), Alex Duval (1) - Molecular and clinical characterization of metastatic
colorectal cancer with microsatellite instability
(1) INSERM, Unité Mixte de Recherche Scientifique 938, Centre de Recherche Saint-Antoine, Equipe B
Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, 184 rue
du Faubourg Saint-Antoine, Paris 75012, France
(2) Department of Medical Oncology, Hospital Saint-Antoine, APHP, 184 rue du Faubourg Saint-Antoine,
Paris 75012, France
(3) Department of Pathology, Hospital Saint-Antoine, APHP, 184 rue du Faubourg Saint-Antoine, Paris 75012,
France
[9] DEZAIRE Ambre1,2, Nathalie Ferrand1, Marine Vallet2, Michèle Sabbah1, Anette K. Larsen1,
Soizic Prado2, Alexandre Escargueil1 - Characterization of bioactive molecules derived from
marine microorganisms, interfering with cell dedifferentiation processes observed at the invasive
front of mammary tumors 1INSERM UMR_S 938 Hôpital Saint Antoine Bâtiment Kourilsky 184, rue du Faubourg St Antoine 75571 Paris
Cedex 12 2UMR 7245, MCAM, CNRS, Muséum National d’Histoire Naturelle, 63 Rue Buffon, 75005 Paris, France.
[10] GEORGE Caroline, Martin Holzenberger and Saba Aïd - Suppression of Neuronal IGF
Signaling Protects from Proteotoxicity and Regulates Cell Size-controlling Pathways
INSERM, Centre de Recherche UMR938, Hôpital Saint-Antoine, and Sorbonne Universités, UPMC - Université
Pierre et Marie Curie, 75012 Paris, France.
[11] GOFAS SALAS Elena (1,2) , M. Pâques(2), C. Petit(1) and S. Meimon (1) - Paris’s High Speed
Adaptive Optics Flood Illumination Ophtalmoscope
(1) ONERA, The French Aerospace Lab, Châtillon, France
(2) CIC 1423, INSERM, Quinze-Vingts Hospital, Paris, France
[12] GREENE Malorie, Ada COLLURA, Alex DUVAL - Consequences of Coding Microsatellite
Instability in Colorectal Cancer: The balance between Transformators and Survivors genes. INSERM, U938
[13] HIRSCH Pierre, TANG, R., FAVA, F., MARZAC, C., DOUAY, L. and DELHOMMEAU, F. - A
phylogenetic strategy for minimal residual disease evaluation in acute myeloid leukemia
AP-HP Hôpital Saint-Antoine, CDR Saint-Antoine
[14] HUR Justine*, Claire KANONY-TRUC #, Thierry CLERC #, Isabelle LIMON* and Régis BLAISE -
Effects of omega-3 fatty acid on cerebrovascular alterations and inflammation in Alzheimer's
disease.
* UMR 8256 Biological Adaptation and Ageing, Université Pierre et Marie Curie, 7 quai Saint Bernard, 75252
Paris, France
# Institut de Recherche Pierre Fabre, 3 avenue Hubert Curien, 31035 Toulouse, France.
[15] LAVIGNE Jeremy, Valérie Buard, Frédéric Soysouvanh, Fabien Milliat and Agnès François -
Consequences of total or endothelial-specific PAI-1 deletion on radiationinduced lung damage
in mice. Institute for Radiological Protection and Nuclear Safety, Fontenay-aux-Roses, France
[16] LIU Jin - The influence of Neurotensin/Neurotensin receptor 1 complex on chemotherapy in
ovarian cancer
INSERM UMR-S 1007
[17] LIU Yuanhui - Role of Small ArfGAP-1 (SMAP1), an Arf6-specific GAP, on EGFR signaling upon
stimulation with various EGFR ligands in the Hep3B hepatocellular carcinoma human cell line
INSERM U938
[18] LOBE Cindy, Vaquero, J., Aoudjehane, L. and Fouassier, L. - Function of cancer-associated
fibroblasts in therapeutic sensitivity to anti-EGFR in cholangiocarcinoma
INSERM, UPMC, La Ligue contre le Cancer
[19] LOISEAU Camille and Laurence Bodineau - Enhancement of the respiratory response to
metabolic acidosis in newborn rat by a progestin. Possible involvement of orexin neurons.
UMR_S 1158 UPMC Neurophysiologie Respiratoire Expérimentale et Clinique - 91 Boulevard de l'Hôpital
Faculté de Médecine de l'Université Pierre et Marie Curie - Site Pitié Salpêtrière
[20] MAREK Veronika*, K. Kessal*, E. Reboussin*, L. Riancho*, G. Rabut**, A. Reaux-Le Goazigo*,
A-L. Raveau*, S. Melik-Parsadaniantz*, C. Baudouin **, T. Villette*** and A. Denoyer** - Clinical,
cell and genomic investigation of the role of light in the dry eye disease
* Paris Vision Institute, UMRS 968 (INSERM, UPMC University of Paris, CNRS), Paris, France
** Quinze-Vingts National Ophthalmology Hospital, Paris, France
*** Essilor International, R&D Department, Paris, France
[21] MEJECASE Cécile1, Caroline Laurent-Coriat2, Saddek Mohand-Saïd1,2, Aline Antonio1,2, Fiona
Boyard1, Christel Condroyer1, Steven Blanchard3, Mélanie Letexier3, Jean-Paul Saraiva3, Jose-
Alain Sahel1,2,4,5,6, Isabelle Audo1,2,4,5* and Christina Zeitz1* - Identification of a novel homozygous
mutation confirms the implication of GNAT1 in rod-cone dystrophy 1Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, 17 rue Moreau, 75012 Paris,
France. 2CHNO des Quinze-Vingts, DHU Sight Restore, INSERM-DHOS CIC1423, 28 rue de Charenton, 75012 Paris,
France. 3IntegraGen SA, Genopole, CAMPUS, 1 bat G8 FR-91030 EVRY, Paris, France 4Institute of Ophtalmology, University College of London, London, United Kingdom. 5Fondation Ophtalmologique Adolphe de Rothschild, Paris, France. 6Academie des Sciences, Institut de France, Paris, France.
*These authors contributed equally to this work, both are corresponding authors
[22] PECKEU Laurène1, Véronique Sazdovitch3, Nicolas Privat1, Arlette Welaratne2, Jean-Louis
Laplanche4, Danielle Seilhean3, Armand Perret-Liaudet5, Jean-Philippe Brandel1,2 and Stéphane
Haïk1,2,3 - Iatrogenic CJD after human GH treatment in France: effect of sex, dose and genetics
on the susceptibility of a possible infection by a V2 sCJD strain 1Institut du cerveau et de la moelle épinière (ICM) - Team "Alzheimer's
and Prion diseases"Inserm UMR-1127/CNRS UMR 7225, Université Pierre & Marie Curie - Paris 6 2AP-HP, Cellule Nationale de Référence des maladies de Creutzfeldt-Jakob, Groupe Hospitalier Pitie-
Salpêtrière, Paris, France 3AP-HP, Laboratoire de Neuropathologie R Escourolle, Groupe Hospitalier Pitie-Salpêtrière, Paris, France 4UF de Génétique Moléulaire, pôle B2P, Hôpital Lariboisière, Paris, France 5Hospices Civils de Lyon–Laboratoire Diagnostic Maladies à Prions; CNRS, Inserm, UCB Lyon1, Centre de
Recherche en Neurosciences de Lyon, BioRan, Bron, France.
[23] PHAM Thi Minh Tam1, Mona Munteanu1,2, Yen Ngo2, An Ngo2, Valentina Peta1,2, Luckina
Elena3, Djamel Elaribi3, Muriel Legroux3, Noemi Seurat3, Léa Verglas3, Thierry Poynard1,3 and Olivier
Lucidarme3 - Evaluation of combination ultrasound, shear wave elastography, and serum
biomarkers in the ultra-early diagnosis of hepatocellular carcinoma 1University Pierre Marie Curie, UMR_S 938, Research Centre Saint-Antoine; 2Research Unit, Biopredictive, Paris, France; 3Groupe hospitalier Pitie-Salpêtrière.
[24] SIQUEIROS Lourdes1,3, Hugo Charles-Messance1, Rodrigo Bolaños-Jimenez4,5, Cecilia
Montañez3, José Alain Sahel1,2, Alvaro Rendon1, Ramin Tadayoni1,6, Audrey Giocanti-Aurégan7 -
Role of Dexamethasone preventing Müller glial cells swelling. 1Institut de la Vision/INSERM/UPMC Univ Paris 06/CNRS/CHNO des Quinze-vingts, Paris, France. 2Fondation Ophtalmologique Adolphe de Rothschild, Paris, France. 3Genetics and Molecular Biology Dept, CINVESTAV, Zacatenco unit, México City. 4Association to prevent blindness in Mexico, Dr. Luis Sanchez Bulnes Hospital, México City. 5Ophthalmology Department, Regional Hospital, Adolfo López Mateos, ISSSTE, México City 6Ophthalmology Dept, Hôpital Lariboisière, AP-HP, Univ Paris Diderot, Paris, France. 7Ophthalmology Dept, Avicenne hospital, 125 rue de Stalingrad 93000 Bobigny.
[25] SOYSOUVANH Fréderic and Milliat Fabien - Endothelial senescence induced by radiation
and effects on healthy tissues
Institut de Radioprotection et de Sûreté Nucléaire (IRSN).
[26] VAN EEGHER Sandy, Maria-Luisa Perez-Lozano, Danièle Citadelle, Audrey Pigenet, Francis
Berenbaum and Xavier Houard - Consequences of hypertrophic chondrocyte differentiation on
osteochondral angiogenesis in osteoarthritis
INSERM UMR-S 938, UPMC, Saint Antoine research center, F-75571 Cedex 12, Paris, France.
Department of Rheumatology and “Inflammation-Immunopathology-Biotherapy” (DHU i2B), AP-HP Saint-
Antoine Hospital, F-75012 Paris, France.
POSTERS
Wednesday, 25th May 2016 – 15:30 to 16:45
[27] BATAILLE Aurélien2, P. Galichon2, N. Chelghoum1, B. Mohand-Oumoussa1, MJ. Ziliotis2, I. Sadia2,
N. Simon2, D. Legouis2, E. Rondeau2 and A. Hertig2 - Acceleration of renal fibrogenesis following
acute kidney injury: insights from the transcriptome of proximal tubules isolated ex vivo 1Plate-forme P3S, Faculté de Médecine Pierre & Marie-Curie, Paris, France 2Inserm UMR_S 1155, Paris, France
[28] BAUM David Marcel1, M Saussereau1, F Jeton2, N Voituron2, C Planès2, P Cardot1, L Bodineau1,
MN Fiamma1 - Obstructive sleep apnea – affecting serotonin signaling without affecting serotonin? 1UMR_S1158 Inserm-Université Pierre et Marie Curie - Neurophysiologie Respiratoire Expérimentale et Clinique -
Physiologie et Plasticité du Contrôle Respiratoire, Faculté de Médecine Pierre et Marie Curie site Pitie-
Salpêtrière - 91 Boulevard de l'Hôpital - 75634 Paris cedex 13, France 2Laboratoire HYPOXIE & POUMON - EA2363 - Université Paris 13, Sorbonne Paris Cite - 74 rue Marcel Cachin -
93017 BOBIGNY Cedex, France.
[29] BEURIOT Adeline, Catherine Eichel, Florent Louault, Alain Coulombe, Stéphane Hatem and Elise
Balse - Involvement of CASK protein domains in the down regulation of the sodium channel Nav 1.5
in cardiomyocytes INSERM UMRS_1166, Université Pierre et Marie Curie, Paris, France
[30] BOITARD Solène, Pierre Joanne, Maria Kitsara, Hany Naemetalla, Valérie Vanneaux, Mathieu
Pernot, Jérôme Larghero, Patricia Forest, Yong Chen, Philippe Menasché and Onnik Agbulut -
Nanofibrous Clinical-grade Collagen Scaffolds Seeded With Human Cardiomyocytes Induces
Cardiac Remodeling In Dilated Cardiomyopathy
University Pierre et Marie Curie, Paris Descartes, Ecole Normale Supérieure, Saint-Louis Hospital, BioM'up
industry, Georges Pompidou European Hospital, Langevin institut.
[31] CAMPION Sébastien, X. Navarro , M. Chavez, P. Pouget, T. Similowski* and M. Raux - Respiratory
discomfort assessment with visual evoked potentials.
INSERM UMR_S 1158 : CAMPION, SIMILOSWKI, RAUX
INSERM UMR_S 975 : NAVARRO, CHAVEZ, POUGET
Département d'Anesthesie-Réanimation, GHPS : RAUX
Pneumologie et Réanimation Médicale, GHPS : SIMILOWSKI
[32] DAHER Marie-Thérèse (1), Raphael Riclet (2), Olivier Rohr (2), Pedro Bausero (1), Pentao Liu (3),
Zhenlin Li (1) and Ara Parlakian (1) - Bcl11b, a transcriptional repressor: Its Role in cardiac
homeostasis and hypertrophy
(1) IBPS, Biological Adaptation and Ageing, UMR 8256, CNRS, INSERM U1164, Université Pierre et Marie Curie,
PARIS, FRANCE
(2) Université de Strasbourg, Strasbourg, FRANCE
(3) Wellcome Trust Institute, Cambridge, UK
[33] DELOUX Robin and Mathias Mericksay - Role of NAD/Nmrk2 signaling pathway in exercise
response during ageing
UPMC
[34] DESBOIS Anne-Claire, M Garrido, A Leroyer, J Gaudric, C Comarmond, D Klatzmann, P Fourret,
L Chiche, F Koskas, G Kaplanski, P Cacoub and D Saadoun - Interleukin 33 in large vessels
vasculitis.
IINSERM UMR_S 959 I3
[35] ESCRIBANO VAZQUEZ Unai and CHERBUY Claire - The role of a commensal Escherichia coli in
the interactions within microbiota-intestinal epithelium
INRA
[36] HAMMOUDI Nadjib, Alexandre Ceccaldi; Stéphane Hatem; François Lionnet; Katia Stankovic
Stojanovic; Jean-Sébastien Hulot and Richard Isnard - Cardiac dysfunction is the main mechanism
of aggravation of exercise intolerance in homozygous sickle cell disease patients.
UMRS INSERM-UPMC 1166 & ICAN
University Paris 6, Faculté de Médecine Pierre et Marie Curie, Paris, France
Department of Cardiology, Assistance Publique – Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris, France
[37] JEZIOROWSKA Dorota1,2, Vincent Fontaine1, Charlene Jouve1, Louise Greetham1 and Jean-
Sebastien Hulot1,2 - Direct comparison of iPS monolayer vs. aggregation-based differentiation
protocols 1ICAN Institute, Paris, France 2UMRS 1166
[38] KORMANN Raphael, N. Prakoura, P. Kavvadas and C. Chatziantoniou - Inhibition of periostin
protects against the nephrotoxic serum nephritis in mice.
UMR1155
[39] LIABOTIS Athanasia1, Elisa Gomez-Perdiguero1, Ariane Galaup1, Clément Faye2, Sylvie Ricard-
Blum2, Catherine Monnot1 and Stéphane Germain1 - Molecular mechanisms of ANGPTL4-induced
regulation of vascular integrity 1Centre Interdisciplinaire de Recherche en Biologie, INSERM U1050, Collège de France 2Institut de Biologie et Chimie des Protéines, UMR 5086 CNRS - Université Lyon 1
[40] MAMELLE Elisabeth1,2,3*, Naila El Kechai4, Benjamin Granger2,5, Olivier Sterkers1,2,3, Amélie
Bochot4, Florence Agnely4, Evelyne Ferrary1,2,3 and Yann Nguyen1,2,3 - Effect of middle ear applied
dexamethasone gel on hearing after manual or motorized cochlear implantation in guinea pig 1UMR S-1159, Inserm / UPMC, “Minimally invasive robot-based hearing rehabilitation”, 75013 Paris France 2Sorbonne University, UPMC, Paris 6, Paris, France 3AP-HP, Pitie-Salpêtrière Hospital, Otolaryngology Department, Unit of Otology, Auditory implants, and Skull
base surgery, 75013 Paris, France 4Institut Galien Paris Sud, CNRS 8612, Univ. Paris-Sud, Paris-Saclay University, 92290 Chatenay-Malabry, France 5AP-HP, Pitie-Salpêtrière Hospital, Department of Public Health, 75013 Paris, France
[41] PAIVA Solenne, Pierre Joanne and Onnik Agbulut - Epigenetic factors for enhanced maturation
of cardiomyocytes derived from human pluripotent stem cells for cardiac tissue engineering
Université Pierre et Marie Curie - Paris 6
[42] PERRA Lea, Viviane Balloy, Sarah Fedele, Harriet Corvol, Michel Chignard and Loic Guillot - Role
of CHAC1 (ChaC Glutathione-Specific Gamma-Glutamylcyclotransferase 1) in the modulation of
CF (Cystic Fibrosis) bronchial epithelial cell response infected with Pseudomonas aeruginosa
INSERM, UMR_S 938, CDR Saint-Antoine, Paris, FRANCE, Sorbonne Universités, UPMC Univ Paris 06, UMR_S 938,
CDR Saint-Antoine, Paris, FRANCE, Pneumologie pédiatrique, AP-HP, Hôpital Trousseau, Paris, France.
[43] RAGOT Hélène, Sabine Guinemer, Inès Da Costa, Evelyne Polidano, Régine Merval, Christos
Chatziantoniou2 and Jane-Lise Samuel - Notch3 null mice show deficient cardiac adaptation to
moderate exercise
UMRS 942, Hôpital Lariboisière, PARIS 2UMRS 1155, Hôpital Tenon, PARIS
[44] RAHHAL Amer1, Slawomir Kusmia2, Fabrice Atassi1, Myriam Berthet1, Alban Redheuil2,Nadjia
Kachenoura2 and S. N. Hatem1 - Role of Epicardial Adipose Tissue in the Pathophysiology of Atrial
Fibrillation 1UPMC Univ Paris 06, INSERM 1166, Sorbonne Universities, Paris. 2UPMC Univ Paris 06, INSERM 1146, CNRS 7371, Laboratoire d’Imagerie Biomédicale, Sorbonne Universities,Paris.
[45] ROSENBAUM David (1,2,3), Antonio Gallo (1,2), Alessandro Mattina (1,2), Edouard Koch (4),
Florence Rossant (5) Nadjia Kachenoura (2,3), Michel Paques (4), Alban Redheuil (2,3,6) and Xavier
Girerd (1,3) - Retinal Arterioles Wall-To-Lumen-Ratio Changes in Humans as Assessed by Adaptive
Optics Camera
(1) Preventive Cardiovascular Unit, Groupe Hospitalier Universitaire Pitie-Salpêtrière, Assistance Publique-
Hôpitaux de Paris, Paris, France.
(2) Sorbonne Universités, UPMC Univ Paris 06, INSERM 1146, – CNRS 7371, Laboratoire d’imagerie Biomédicale,
F-75013, Paris, France.
(3) Institute of Cardiometabolism and Nutrition, ICAN, Paris, France
(4) Unité INSERM 968 Institut de la vision - Centre d’Investigation Clinique 503 Centre Hospitalier National des
Quinze-Vingts, Assistance Publique-Hôpitaux de Paris, Paris, France.
(5) ISEP, Paris
(6) Département d’imagerie cardiovasculaire et de radiologie interventionnelle, Pôle Imagerie - Groupe
Hospitalier Pitie-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France.
[46] SALEM Joe-Elie MD ‡§, Marine Germain*‡, Beny Charbit*, MD, PHD#, Pascal Voiriot, MD II,
Bruno Lebourgeois, MD§, Eric Dasque, RN §, Jean Waldura, PHD‖II, David-Alexandre Tregouet,
PHD‡, Christian Funck-Brentano,MD-PHD‡§ and Jean-Sébastien Hulot, MD-PHD ‡§ - GENomE Wide
Analysis of Sotalol-induced IKr inhibition during ventricular REPOLarization, “GENEREPOL study”: Lack
of common variants with large effect sizes.
‡ Sorbonne-Universités, UPMC Univ Paris 06, INSERM, UMRS-1166, Institute of Cardio metabolism and Nutrition
(ICAN), Paris, France
§ AP-HP, CIC-1421-Paris-Est, Pitie-Salpêtrière Hospital, F-75013, Paris, France
II‖ Cardiabase-Banook group, Nancy, France.
# Anesthesia-Reanimation department, Hôpital Robert Debré, Reims, France.
[47] SERBIN Bettina, Mumtaz R, Trepiccione F, Hennings JC, Huebner AK, Ullah SA, Paunescu T,
Capen D, Lashhab RM, Mouro-Chanteloup I, Alper SL, Wagner CA, Cordat E, Brown D, Eladari D
and Hübner CA - Type A intercalated cell depletion and V-ATPase mistargeting in AE1 R607H
knock-in mice modeling human dominant distal renal tubular acidosis 1Institute of Human Genetics, Jena University Hospital, Friedrich Schiller Universität, Jena, Germany 2INSERM U970, Paris Cardiovascular Research Center ; Université Paris Descartes, Department of Physiology,
European Hospital Georges Pompidou, Paris, France 3Department of Physiology, University of Alberta, Edmonton, Alberta, Canada 4Center for Systems Biology, Massachusetts General Hospital, Boston and Program in Membrane Biology,
Harvard Medical School, Boston and Division of Nephrology, Harvard Medical School, Boston, USA 5Institut National de la Transfusion Sanguine, Paris, France, Inserm, UMR_S665, Paris, France, Université Paris
Diderot, Sorbonne Paris Cité, Paris, France, Laboratory of Excellence GR-Ex., Paris, France 6Renal Division and Molecular and Vascular Medicine Division, Beth Israel Deaconess Medical Center;
Department of Medicine, Harvard Medical School, Boston, USA 7Institute of Physiology, University of Zurich, Zurich, Switzerland
[48] SONNEVILLE Florence¹, M. Ruffin¹, P. Le Rouzic¹, H. Corvol¹ and O. Tabary¹ - miR-9 and ANO1:
therapeutic targets in cystic fibrosis
CDR Saint-Antoine, Paris, France
[49] TANNOUS Cynthia1, Jocelyne Blanc1, Nathalie Mougenot2-3, Arnaud Ferry2, Stéphane Hatem2-3,
Zhenlin Li1 and Mathias Mericskay1 - Role of nicotinamide riboside kinase 2 in dilated
cardiomyopathy 1Institute of Biology Paris-Seine, Université Pierre et Marie Curie Paris 6, Dept of Adaptation and Ageing Biology
(CNRS UMR 8256 / Inserm ERL U1164) (Paris, France) 2ICAN, Plateau d'Expérimentation Coeur, Muscle, Vaisseaux, GH Pitié Salpétrière, Université Pierre et Marie
Curie Paris 6 (Paris, France) 3ICAN, Génétique, Physiopathologie & Pharmacologie Cardiovasculaire INSERM U956, Université Pierre et
Marie Curie Paris 6 (Paris, France)
[50] TIAN Lei - Role of integrin αv and transcription factor SRF in the vascular stiffness
UPMC Univ Paris 06, CNRS UMR8256/INSERM ERL U1164
[51] TORRES LAZO Victor Renato MD1,2,3, Guillaume Kazmitcheff PhD1,3,4, Daniele De Seta MD1,2,3,
Evelyne Ferrary MD, PhD1,2,3, Olivier Sterkers MD, PhD1,2,3, Yann Nguyen MD, PhD1,2,3 - Improvement of
the variability of the insertion axis to the scala tympani by a robotic semi-automatic system in
cochlear implantation 1UMR-S 1159 “Minimally Invasive Robot-based Hearing Rehabilitation”, Inserm, Paris 6 UPMC, Paris France 2Sorbonne Universities, UPMC Univ. Paris 6, Paris, France 3Otolaryngology Department, Unit of Otology, Auditory Implants and Skull Base Surgery, AP-HP, Pitié-Salpêtrière
Hospital, Paris, France 4Shacra Inria, Lille Nord-Europe, Université Lille-1, Lille, France
[52] VOISIN Sarah, Wu Q, Jouin M, Pattou F, Six MF, Patrice A, Junien C, Gabory A - Methylome and
transcriptome analysis of abdominal muscle in type 2 diabetic women
UMR BDR, INRA, Domaine de Vilvert, 78350 Jouy en Josas, France. Ecole Doctorale 394 “Physiologie,
physiopathologie et thérapeutique”,Université Pierre et Marie Curie, 75252 Paris, France
POSTERS
Thursday, 26th May 2016 – 10:15 to 11:30
[1] BALBINO Bianca, Pierre Bruhns and Laurent Reber - Pathways of peanut anaphylaxis in a
'humanized' mouse model
Institut Pasteur
[2] BONNET Benjamin1,2,3,4, James Vigneron1,2,3, Béatrice Levacher1,2,3, Thomas Vazquez1,2,3, Fabien
Pitoiset1,2,3, Faustine Brimaud1,2,3, Guillaume Churlaud1,2,3,4, David Klatzmann1,2,3,4, Bertrand
Bellier1,2,3,4 - Low-dose interleukin-2 induces regulatory T-cell mediated control of experimental
food allergy 1Sorbonne Universités, UPMC Univ Paris 06, UMRS_959, I3, F-75013, Paris, France 2INSERM, UMRS_959, I3, F-75013, Paris, France 3CNRS, FRE3632, I3, F-75013, Paris, France 4AP-HP, Groupe Hospitalier Pitie-Salpêtrière, Department of Biotherapies and Clinical Investigation Center in
Biotherapy, F-75013, Paris, France.
[3] CANESI Fanny, Vimala Diderot, Dominique Couchie, Mustapha Rouis & Khadija El Hadri -
Thioredoxin-Mimetic Peptides: New Promising Therapeutic Strategyfor the Treatment of
Cardiovascular Diseases
UMR 8256 - B2A - Biological Adaptation and Ageing ; UPMC ; INSERM ; CNRS
[4] CONART Jean-Baptiste, Xavier Guilloneau, Pascale Massin and Florian Sennlaub - Cone
segment loss in retinal detachment
Sorbonne Université, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, Unité 968, 17 rue Moreau, 75012
Paris, France.
[5] DAS Mrinmoy, Maxime Lecerf, Srini V Kaveri and Jagadeesh Bayry - Induction of autophagy in
immune cells by Intravenous Immunoglobulin.
Centre de Recherche des Cordeliers, Equipe 16 - Immunopathology and therapeutic immunointervention,
Paris, F-75006, France
[6] DIALLO Mariama1, Samri, A.1, Even, S.1, Charpentier, C.2, Matheron, S.3, Brinvezinet, F.2, Autran,
B.1 - Distribution of HIV-2 Reservoir in Cd4 + Cells Patient Infected with HIV-2 1Sorbonne Universités, UPMC Univ Paris 06, CIMI - Paris, F-75013, France; Inserm, U1135, CIMI- Paris, Paris, F-
75013, France; AP-HP, Hôpital Pitié-Salpêtrière, Département d’Immunologie, Paris, F-75013, France 2AP-HP, Hôpital Bichat-Claude Bernard, Laboratoire de Virologie EA 4409, Paris, F- 75018, France ; Université
Paris-Diderot, Sorbonne Paris-Cité, Faculté de Médecine. 3AP-HP, Hôpital Bichat-Claude Bernard, Service de Maladies infectieuses et tropicales, Paris, F- 75018,
France ; Université Paris-Diderot, Sorbonne Paris-Cité, Faculté de Médecine.
[7] DIVOUX Jordane, Vallion, R., Ronin, E., Lubrano di Rocco, M., Preato, C., Gregoire, S., Marodon,
G., Banderas, A. and Salomon, B. - Obesity induced inflammation: impacts on immune cells in
visceral adipose tissue
CIMI U1135
[8] DONG Yuan*†, J. Lagarde‡, H. Corne‡, Y. Chantran*†, P. Aucouturier*†, G. Dorothée†, M.
Sarazin‡ and C. Elbim*† - Phenotypic and functional characterization of neutrophils in Alzheimer
disease: association with disease severity
*Sorbonne Universités, UPMC Univ Paris 06, Paris, France ;
†INSERM, Centre de Recherche Saint-Antoine, UMR-S 938, Paris, France ;
‡AP-HP, Hôpital Saint-Anne, Unité de neurologie de la mémoire et du langage, Paris, France. [9] DRARENI Karima, Amine Toubal, Rapahelle Ballaire, Eckardt Treuter and Nicolas Venteclef -
Epigenomic control of adipose tissue function and energy metabolism in obesity and type 2
diabetes
Equipe 8 - pathogenèse cellulaire et clinique du diabète
[10] EYMARD Florent1,2, Audrey Pigenet1, Danièle Citadelle1, Joan Tordjmann3, Charles-Henri
Flouzat Lachaniette4, Karine Clément3, Francis Berenbaum1,5, Xavier Chevalier2 and Xavier
Houard1 - Knee and hip intra-articular adipose tissues share a common phenotype in osteoarthritis 1INSERM UMR-S 938, UPMC, Saint Antoine research center, F-75571 Cedex 12, Paris, France. 2Department of Rheumatology, AP-HP Henri Mondor Hospital, F-94010, Créteil Cedex, France. 3INSERM U1166, UPMC, Cordeliers research center, 75006, Paris, France 4Department of Orthopedic Surgery, AP-HP Henri Mondor Hospital, F-94010, Créteil Cedex, France. 5Department of Rheumatology and “Inflammation-Immunopathology-Biotherapy” (DHU i2B), AP-HP Saint-
Antoine Hospital, F-75012 Paris, France.
[11] GALEOTTI Caroline (1, 2, 3, 4), Hedge P (1,3), Das M (1,2,3), Stephen-Victor E (1,2,3), Canale F
(1,3), Munoz M (1,3), Sharma VK (1,3), Dimitrov JD (1,2,3,5), Kaveri SV (1,2,3,5,6) and Bayry J
(1,2,3,5,6) - Heme oxygenase-1 is dispensable for the anti-inflammatory activity of intravenous
immunoglobulin
(1) Institut National de la Santé et de la Recherche Médicale Unité 1138, Paris, F-75006, France
(2) Sorbonne Universités, UPMC Univ Paris 06, UMRS 1138, Paris, F-75006, France
(3) Centre de Recherche des Cordeliers, Equipe-Immunopathology and theraeutic immunointervention,
Paris, F-75006, France
(4) department of Pediatric Rheumatology, National Referral Centre of Auto-inflammatory Diseases, CHU de
Bicêtre, Le Kremlin Bicêtre, F-94270, France
(5) Université Paris Descartes, Sorbonne Paris Cité, UMRS 1138, Paris, F-75006, France
(6) International Associated Laboratory IMPACT , National Institute of Immunohaematology, Mumbai, 400012,
India
[12] GEA-MALLORQUI Ester, Mabel Jouve, Nicolas Ruffin, Laurent Zabloki, Mathieu Maurin and
Philippe Benaroch - HIV-2 infection in Human Macrophages.
U932 Institut Curie.
[13] GONNET Jessica1, Weiss L.1,2, Boccara D.1,3, Cardinaud S.1, Yahia N.1, Dufossée M.1, Wagner
R.4, Verrier B.5, Moris A.1, Vogt A.1,2,Mimoun M.3, Combadière B.1 and Perrin H.1 - IL-32 role in
antigen-specific T cell responses after MVA administration in human skin 1Centre d’Immunologie et des Maladies Infectieuses-Paris (Cimi-Paris), Inserm U1135, Sorbonne Universités
UPMC université Paris 06 UMRS CR7 2Clinical Research Center for Hair and Skin Science, Department of Dermatology and Allergy, Charité-
Universitätsmedizin Berlin, Berlin, Germany 3Service de chirurgie plastique reconstructrice, esthétique, centre des brûlés, hopital Saint-Louis, Assistance
Publique Hôpitaux de Paris 4Fachgruppe Physik, Bergische Universit¨at Wuppertal, 42097 Wuppertal, Germany 5Institut de Biologie et Chimie des proteins UMR 5305, CNRS/Université de Lyon.
[14] Bagirath Gangadharan1,2,3, ING Mathieu1,2,3, Sandrine Delignat1,2,3, Ivan Peyron1,2,3, Maud
Teyssandier1,2,3, Srinivas V Kaveri1,2,3 and Sébastien Lacroix-Desmazes1,2,3 - Role of the C domains in
the immunogenicity of therapeutic factor VIII in hemophilia A 1Sorbonne Universités, UPMC Univ Paris 06, UMR S 1138, Centre de Recherche des Cordeliers, F-75006, Paris,
France; 2INSERM, UMR S 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France; 3Université Paris Descartes, Sorbonne Paris Cité, UMR S 1138, Centre de Recherche des Cordeliers, F-75006,
Paris, France.
[15] JAILLET Cyprien*, Willy Morelle°, Pierre Martinez°, Marie-Christine Slomianny°, Valérie Buard*,
Fanny Caffin*, Marc Benderitter*, Christian Slomianny°°, Anne-Sophie Lacoste°°, François
Foulquier°, Agnès François*, Fabien Milliat*, Fabrice Allain° and Olivier Guipaud* - Role of
endothelial cell glycosylation in the initiation and development of radiation tissue injury
*IRSN, PRP-HOM/SRBE/L3R, 92260 Fontenay-aux-Roses;
°UGSF, UMR8576
°°Bio Imaging Center, Inserm U1003, Université Lille 1, 59655 Villeneuve D’Ascq, France
[16] Le MOIGNIC Aline, Maude Guillot-Delost, Claude Baillou, Patrick Midoux, François Lemoine
and Véronique Mateo - Preclinical validation of new therapeutic anti-cancer vaccine targeting
dendritic cells by using RNA modified lipopolyplexes
CIMI - Centre de recherche d'Immunologie et Maladies infectieuses ; UMRS CR7, INSERM U1135, CNRS ERL
[17] Scott D. Speer, LI Wu Zhi, Béatrice Payelle-Brogard, Sofija Buta, Erminia Rubino, Sara Löchte,
Stephan Wilmes, Jacob Piehler, Dusan Bogunovic and Sandra Pellegrini - Fine Tuning of Type I
Interferon Response in Humans and Mice
Institut Pasteur, Paris, France ; Icahn School of Medicine at Mount Sinai, NY, NY, USA ; University of Osnabrück,
Osnabrück, Germany
[18] LUBRANO DI RICO Martina, Sylvie Gregoire, Benoit Salomon - Role of TNFR family on regulatory
T cells.
INSERM-CNRS-UPMC
[19] LUQUE Yosu1,2,3, Dominique Cathelin1,2, Sophie Vandermeersch1,2, Xiaoli Xu1,2, Julie Sohier1,2,
Sandrine Placier1,2, Alexandre Hertig1,2,3, Jean-Christophe Bories4, Florence Vasseur5, Fabien
Campagne6, James P. Di Santo7, Christian Vosshenrich7, Eric Rondeau1,2,3 and Laurent
Mesnard1,2,3,6 - Glomerular common gamma chain confers B and T cell-independent resistance to
glomerulonephritis 1Sorbonne Universités, UPMC Univ Paris 06, UMR_S 1155, “Rare and Common Kidney Diseases, Matrix
Remodeling and Tissue Repair”, F-75005, Paris, France 2Inserm UMR 1155, “Rare and Common Kidney Diseases, Matrix Remodeling and Tissue Repair”, Hôpital
Tenon, F-75020, Paris, France 3APHP, Urgences Néphrologiques et Transplantation Rénale, Hôpital Tenon, F-75020, Paris, France 4Inserm UMR 1126, Institut Universitaire d'Hématologie, Hôpital St. Louis, Paris, France 5Inserm U1020, Université Paris Descartes, 75014 Paris, France 6Weill Medical College of Cornell University, Institute of Computational Biomedicine, New York, NY 10065, USA 7Institut Pasteur, Unité Immunité innée and Inserm U668, 75724 Paris, France
[20] MONSEL Antoine, Lucrèce Aimade, Olivier Langeron, David Klatzmann, Michelle Rosenzwajg -
Temporal and compartment dynamics of immune phenotypes in acute respiratory distress
syndrome Multidisciplinary Intensive Care Unit, Department of Anesthesiology and Critical Care, La Pitie-Salpêtrière
Hospital, Assistance Publique-Hôpitaux de Paris
Laboratoire Immunologie-Immunopathologie-Immunothérapie Equipe ImmunoPhysiopathologie (iP) UPMC
UMR 7211 - CNRS FRE3632 - INSERM U959
[21] OUHACHI Melissa, Martine Moreau, Philippe Lesnik, Thierry Huby, Emmanuel Gautier - IRF4-
dependent CD11b+ dendritic cells controls the polarization of Th cells in atherosclerosis.
INSERM U1166.
[22] RONIN Emilie, Rouers A, Pouchy C, Grégoire S, Zaragoza B, Burlion A, Weih F, Baeyens A,
Salomon B - Role of NF-kB in the biology of FoxP3+ regulatory T cells at steady state and during
inflammation
UPMC/Inserm/CNRS
[23] TCHOUKAEV Anastasia1,4, J. Taytard1,3,4, C. Rebeyrol1,4, F. Sonneville1,4, P. Bardin1,4, D. Debray1,
N. Rousselet1,4, S. Blouquit-Laye2, L. Guillot1,4, H. Corvol1,3,4, N. Chignard1,4, O. Tabary1,4 and P. Le
Rouzic1,4 - Regulation of corticosteroid-binding globulin (CBG) in the inflammatory context of
cystic fibrosis. 1UMR_S938 Inserm, 2Université Versailles, Saint-Quentin en Yvelines, 3Hôpital Armand Trousseau, Paris, 4Université Paris 06, Paris.
[24] TOUHAMI Sara, Sébastien Augustin, Xavier Guillonneau and Florian Sennlaub - Age-related
Macular Degeneration and Sleep Apnea Institut de la Vision, UMRS 968
[25] TRAN Sophie, Lucie Poupel, Melissa Ouhachi, Thierry Huby, Wilfried Le Goff, Emmanuel Gautier
- Deciphering the role of liver macrophage subsets in cardiometabolic diseases.
INSERM UMRS_1166
[26] URRUTIA Alexandra1,2,*, Darragh Duffy1,2,3,*, Vincent Rouilly3, Céline Posseme3, Raouf Djebali3,
Gabriel Illanes3,4,5, Valentina Libri3, Benoit Albaud6, David Gentien6, Barbara Piasecka3, Milena
Hasan3, Magnus Fontes4,7*, Lluis Quintana-Murci8,9,*, Matthew L. Albert1,2,3,10,* for The Milieu Intérieur
Consortium† - Standardized whole-blood transcriptional profiling enables the deconvolution of
complex induced immune responses 1Laboratory of Dendritic Cell Immunobiology, Department of Immunology, Institut Pasteur, Paris France 2INSERM U818, Paris France 3Center for Human Immunology, Institut Pasteur, Paris France 4IGDA, Institut Pasteur, Paris France 5Centro de Matemática, Facultad de Ciencias, Universidad de la República, Uruguay. 6Institut Curie, Centre de Recherche, Département de recherche translationnelle, Plateforme de
Génomique, Paris, France 7Centre for Mathematical Sciences, Lund University, Lund, Sweden 8Laboratory of Human Evolutionary Genetics, Department of Genomes & Genetics, Institut Pasteur, Paris
France 9CNRS URA3012, Paris France 10Department of Cancer Immunology, Genentech Inc, San Francisco CA
[27] VILLEGAS VAZQUEZ Jose, Le Panse R, Berrih-aknin S and Dragin N - Expression of Interleukin-23
in Thymuses of Myasthenia Gravis Patients
Center of Research in Myology, Sorbonne Universités, UPMC - Inserm UMRS 974, CNRS FRE3617, Institute of
Myology, G.H. Pitie-Salpêtrière, Paris, France.
[28] ZABLOCKI Laurent1, Aditi Varthaman1, Francois-Xavier Gobert1, Samuel Menzies2, Paul Lehner2,
Nicolas Manel1 and Philippe Benaroch1 - Analysis of the molecular mechanisms of innate immune
response using a genome wide genetic screen.
1Institut Curie-INSERM U9321, 12 rue Lhomond, 75005 Paris, France ; 2Cambridge Institute for Medical Research2, Addenbrooke’s Hospital, Cambridge, United Kingdom
POSTERS
Thursday, 26th May 2016 – 16:15 to 17:30
[29] BERTAUX Audrey, Cabon L., Brunelle M. N. and Susin S. A. - Control of mitochondrial OXPHOS
and metabolism by AIF is essential for hematopoiesis
Centre de Recherche des Cordeliers UMRS 1138
[30] BOUFTAS Nora, Nikalayevich Elvira, Wassmann Katja - Regulation of chromosome
segregation in mammalian oocytes.
Mammalian Oocyte Meiosis -MOM (Wassmann lab)- UMR7622
[31] BRUNEAU Alix1*, Jean-Louis Delaunay1*, Brice Hoffmann2, Anne-Marie Durand-Schneider1,
Véronique Barbu1, Chantal Housset1, Michèle Maurice1, Isabelle Callebaut2, Tounsia Aït Slimane1
- Phenotypic analysis of function-defective ABCB4 mutants: Effect of correcting molecules 1Centre de Recherche saint-Antoine , INSERM/UPMC, 27 rue Chaligny, Paris 75012, France 2IMPMC, UMR7590, CNRS-UPMC, MNHN, IRD, Paris, 75005, France
* Equal contribution
[32] CANLORBE Geoffroy1,2,3, Zhe Wang1, Enora Laas2, Sofiane Bendifallah2,4, Mathieu Castela1,
Marine Lefevre5, Nathalie Chabbert-Buffet1,2, Emile Daraï1,2,3, Selim Aractingi1, Céline Méhats6,7
and Marcos Ballester1,2,3,7 - Identification of microRNA expression profile related to lymph node
status in women with early-stage grade 1–2 endometrial cancer 1INSERM, UMR S 938, University Pierre et Marie Curie, Paris, France; 2Department of Obstetrics and Gynaecology, Tenon University Hospital, Assistance Publique des Hôpitaux
de Paris (AP-HP), University Pierre and Marie Curie, et Paris, Paris, France; 3Institut Universitaire de Cancérologie (IUC), Paris, France; 4INSERM UMR S 707, Epidemiology, Information Systems, Modeling, University Pierre and Marie Curie, Paris,
France; 5Department of Pathology, Tenon University Hospital, University Pierre and Marie Curie, Paris, France
6Cochin Institute, Inserm U1016, CNRS 8104, Université Paris Descartes, Paris, France
[33] COURTIES Alice1, Alain Sautet2, Francis berenbaum1 and Jérémie Sellam1 - The non-neuronal
cholinergic system: a new actor involved in osteoarthritis pathophysiology. 1Rheumatology Department, Saint-Antoine Hospital, Inserm UMR S_938, UPMC Univ Paris 06, Assistance
Publique–Hôpitaux de Paris (AP-HP), Paris, France 2Department of surgical orthopaedic, Saint-Antoine Hospital, Assistance Publique–Hôpitaux de Paris (AP-
HP), Paris, France
[34] DACLAT Rita and Jean-Marc Lacorte - Postprandial modulation of circulating microRNA in
hypertriglyceridemic patients
UMRS Inserm/UPMC 1166-Equipe 4
[35] DALLE Héloïse, Marie Garcia, Tatiana Ledent, Marthe Moldes and Bruno Feve - The role of
adipose glucocorticoid receptor in corticosterone-induced lipodytrophy.
Lipodystrophies génétiques et acquises INSERM-UMR_S 938
[36] GENSER Laurent1,2,6, Sabrina Benaïssa1,3, Adriana Torcivia6, Monique Rousset1,3, Karine
Clément1,2,4, Edith Brot-Laroche1,3 , Armelle Leturque1,3, Sophie Thenet1,3,5* , Christine Poitou1,2,4* -
Impairment of Intestinal Barrier Integrity in Human Obesity: Involvement of Dietary Lipids 1Institute of Cardiometabolism and Nutrition, ICAN, Pitie-Salpêtrière Hospital, Paris, F-7513, France; 2UMR 1166 team 6 INSERM UPMC UPD, Pitie-Salpêtrière Hospital, Paris, F-75013 France 3UMR 1138 INSERM UPMC UPD, Cordeliers Research Center, F-75006 Paris; 4Assistance Publique-Hôpitaux de Paris, Pitie-Salpêtrière Hospital, Heart and metabolism department Paris,
F-75013 France; CRNH-Ile de France, Paris, F-75013 France; 5EPHE, PSL Research University, F-75006 Paris; 6Department of digestive surgery, liver transplantation, Pitie-Salpêtrière Hospital.
[37] GIABICANI Eloïse - Physiopathology of Insulin like growth factor 1 receptor
UMR_S938 Hôpital Armand Trousseau, 26 rue du Dr A. Netter, 75012 Paris
[38] GRANJON David1,2, Olivier Bonny2 and Aurélie Edwards1 - A model of Ca/Pi homeostasis. 1Equipe 3 Métabolisme et Physiologie Rénale, Centre de Recherche des Cordeliers, Paris 2Département de Pharmacologie et Toxicologie, Université de Lausanne, Lausanne, Suisse
[39] HANOUNA Guillaume, Laurent Mesnard, Sophie Vandermeersch, Joëlle Perez, Sandrine
Placier, Jean-Philippe Haymann, Aurélien Bataille, Laurent Baud, Emmanuel Letavernier -
Specific calpain inhibition protects against inflamm-aging.
Sorbonne universites-UPMC Univ Paris 06, UMR S 1155, F-75020, Paris, France ; INSERM, UMR S 1155, F-75020,
Paris, France ; AP-HP, Hôpital Tenon, Explorations fonctionnelles multidisciplinaires 75020, Paris, France
[40] KEMGANG Astrid - Contribution of gut microbiota in Primary Sclerosing Cholangitis (PSC)
Metabolic and biliary fibro-inflammatory diseases of liver (Pr Housset)
[41] LE GUILCHER Camille1,2, Garcin Isabelle1, Tebbi Ali3, Besnard Aurore1, Doignon Isabelle1,
Julien Boris1 and Tordjmann Thierry1 - The purinergic receptor P2X4 regulates liver fibrogenesis
through the modulation of myofibroblast activation and inflammatory response 1INSERM U1174, Université Paris Sud 91400 Orsay ; 2UPMC Université Paris 6 75005; 3 Affymetrix eBioscience 140 B Rue de Rennes,75006 Paris.
[42] LOEUILLARD Emilien, Haquima El Mourabit, Chantal Housset and Axelle Cadoret - Inhibitory
effect of endoplasmic reticulum stress in portal myofibroblasts on liver fibrogenesis
UMRS 938 CDR Saint Antoine Maladies fibro-inflammatoires d’origine métabolique et biliaire
[43] MA Feng - HDL function as an acceptor of surface fragment of TGRL: Mechanisms and
pathophysiological relevance
Biologie intégrative de l'athérosclérose
[44] MESDOM Pierre1, Andrei Baiceanu1,2, Isabelle Hainault1, Marie Lagouge1 and Fabienne
Foufelle1 - The Role of PRDM16 in Liver Fibrosis 1UMRS 1138 Centre de Recherche des Cordeliers, département pathogénèse cellulaire et clinique du
diabète, Paris, France. 2University of Medicine and Pharmacy "Iuliu Hațieganu", Faculty of Pharmacy, Cluj-Napoca, Romania.
[45] MOURI Sarah1,2, H El-Mourabit1,2, C Rey1,2, R Morichon3, D Wendum1,2,4, E Lasnier5, C
Housset1,2,6 , N Weiss1,2,7 and D Thabut1,2,8 - Blood brain barrier permeability is increased in
hepatic encephalopathy related to cirrhosis, through a hyperammonemia-dependent
mechanism 1Sorbonne Universités, UPMC Univ Paris 06, CDR Saint-Antoine & Institute of Cardiometabolism and Nutrition
(ICAN), Paris, France;
2INSERM, UMR_S 938, Paris, France; 3Institut Fédératif de Recherche en Santé, Saint-Antoine IFR-65, Paris, France; 4Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Service d’Anatomo-Pathologie, Paris, France; 5Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Service de Biochimie; 6Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Centre de Référence des Maladies
Inflammatoires des Voies Biliaires (CMR MIVB) & Service d’Hépatologie, Paris, France; 7Assistance Publique- Hôpitaux de Paris, Hôpital Pitié Salpétrière, Unité de Soins Intensifs de Neurologie; 8Assistance Publique-Hôpitaux de Paris, Hôpital Pitié Salpétrière, Service d’Hepato-Gastroentérologie, Paris,
France [46] NICOLAS Anthony1,2, Kamel Mohammedi1,3, Naima Bellili-Muñoz1, Ronan Roussel1,3,4, Samy
Hadjadj5, Michel Marre1,3,4, Gilberto Velho1, Frédéric Fumeron1,4 - T-cadherin gene (cdh13)
polymorphisms and nephropathy in subjects with type 1 diabetes 1INSERM UMRS1138, Paris, France 2Université Pierre et Marie Curie, Sorbonne Universités, Paris, France 3Dept. Of Diabetology, Endocrinology and Nutrition, Bichat Hospital, APHP, Paris, France 4Université Paris Diderot, Sorbonne Paris Cité, Paris, France 5Dept. Of Diabetology and Endocrinology, University Hospital of Poitiers, Poitiers, France
[47] RIBAULT Alexandre, Stephane Flamant, Marc Benderitter and Radia Tamarat - Exosomes
therapeutic efficiency in the treatment of musculo-cutaneous radiation-induced damages
IRSN - Laboratoire de Rehcerhche en Régénération des Tissus Sains Irradiés
[48] ROUILLE THOMAS1,2, Natacha Kadlub3,4, Alexandre How-Kit5, Sylvie Fraitag6, Romain H.
Fontaine1,2, Selim Aractingi1,3,7 and Sarah Guégan1,2,8 - NRAS mutation and downstream signaling
pathways in congenital melanocytic pathways 1INSERM U938, Saint Antoine Research Center, Paris; 2Université Pierre et Marie Curie-Paris VI, Paris; 3Université René Descartes-Paris V, Paris, France; 4Hôpital Necker, Department of Maxillofacial and Plastic Surgery, Paris, France; 5Laboratory for Functional Genomics, Fondation Jean Dausset – CEPH, Paris, France; 6Hôpital Necker-Enfants-Malades, Department of Pathology, Paris; 7Hôpital Cochin, Department of Dermatology, Paris; 8Hôpital Tenon, Department of Dermatology, Paris.
[49] SAGET Sarah1, Lyvianne Decourtye1, Rong Cong1, Marie-Laure Endale2, Marthe Moldes1,
Laetitia Dinard1, David Tregouet2, Bruno Fève1,3, Yves Le Bouc1,4 and Laurent Kappeler1 -
Epigenetic modifications in liver are associated with metabolic alterations in mice born with
IUGR 1Sorbonne Universités, Univ Paris 06 UMR S938 and INSERM, Unité 938 and Institute of Cardiometabolism and
Nutrition (ICAN) and CDR Saint-Antoine, F-75012, Paris, France; 2Sorbonne Universités, Univ Paris 06 UMR S1166, INSERM, Unité 1166 and Institute of Cardiometabolism and
Nutrition (ICAN), F-75013, Paris, France; 3AP-HP, Hôpital Saint Antoine, F-75012, Paris, France; 4AP-HP, Hôpital Armand Trousseau, F-75012, Paris, France;
[50] SANCHEZ Manuel1, K. Mohammedi1,6, N. Bellili-Muñoz1, S. Hadjadj2,3,4, M. Marre1,5,6, R.
Roussel1,5,6 and G. Velho1 - DNA Oxidation and Diabetic Nephropathy in People with Type 1
Diabetes 1INSERM, Research Unit 1138, Centre de Recherche des Cordeliers, Paris, France; 2Université de Poitiers, CIC1402, Poitiers, France; 3CHU Poitiers, pole DUNE, Poitiers, France; 4INSERM, Research Unit 1082, Poitiers, France; 5Diabetology Endocrinology Nutrition, DHU FIRE, Bichat Hospital, Paris, France; 6University Paris Diderot, Department of Medicine, Paris, France
[51] SCHMITT Charlotte1, Thomas Aranias1, Véronique Carrière1, Kévin Garbin1, Maude Le Gall2,
Edith Brot-Laroche1, Armelle Leturque1, Alexandra Grosfeld1 and Patricia Serradas1 - Intestinal
GLUT2 invalidation leads to glucose malabsorption and decreased GLP-1 cell density 1Inserm UMR_S 1138, Centre de Recherche des Cordeliers; Sorbonne universités, UPMC Univ Paris 06;
Sorbonne Cités, UPD Univ Paris 05; F-75006, Paris, France 2Inserm UMR_S 1149, DHU Unity; Sorbonne Cités, UPD Univ Paris 05, F-75890, Paris, France
[52] TOUCH Sothea1,2,3, Christine Poitou1,2,3,4, Magali Fradet3, Laurent Genser1,2,3,4, Aurélie
Gestin1,2,3, Héléna Mosbah1,2,3,4, Judith Aron-Wisnewsky1,2,3,4, Edith Brot-Laroche1,2,5, Michèle
Guerre-Millo1,2,3, Karine Clément1,2,3,4, Sébastien André1,2,3 - Functional interactions between
systemic and intestinal immunity in human obesity 1Sorbonne Universités, UPMC Univ Paris 6, UMRS 1166 and UMRS 1138, Paris, France 2INSERM, U1166 Team 6 Nutriomics, Paris, France, 3Institute of Cardiometabolism And Nutrition, ICAN, Paris, France, 4Assistance Publique Hôpitaux de Paris, AP-HP, Pitié Salpêtrière Hospital, Nutrition department, Paris, France, 5INSERM, U1138 Cordeliers Research Center, Paris, France.
[53] VALLOT Antoine, Ioanna Leontiou, Warif El Yakoubi, Damien Cladière, Eulalie Buffin and
Katja Wassmann - Quality of chromosome attachments is controlled by the spindle assembly
checkpoint in oocytes
Sorbonne Universités, Intitut de Biologie Paris Seine, CNRS UMR7622 Developmental Biology Lab, Paris 75005
France
[54] ZHANG Xufei, Devime F, Maximin E, Blottière H, Heberden C and Douard V. - Role of
intestinal homeostasis in mediating the effect of chronic intake of sugars
NIM--MICALIS--INRA Jouy-en-Josas
CONTACT LIST
1st YEAR PhD student
ATLAS Yoann [email protected]
BALBINO Bianca [email protected]
BANDET Cécile [email protected]
BOTTE Alexandra [email protected]
BOUFTAS Nora [email protected]
BOUGACHA Nadia [email protected]
BOUVET Delphine [email protected]
BRUNEAU Alix [email protected]
CAMPION Sébastien [email protected]
CANESI Fanny [email protected]
COHEN Romain [email protected]
CONART Jean-Baptiste [email protected]
COURTIES Alice [email protected]
COUTURIER Aude [email protected]
DACLAT Rita [email protected]
DAHER Marie-Thérèse [email protected]
DALLE Héloïse [email protected]
DELOUX Robin [email protected]
DIALLO Mariama [email protected]
DIVOUX Jordane [email protected]
DONG Yuan [email protected]
DRARENI Karima [email protected]
ESCRIBANO VAZQUEZ Unai [email protected]
GHEZZAL Sara [email protected]
GOFAS SALAS Elena [email protected]
KORMANN Raphael [email protected]
LATTUCA Benoît [email protected]
LE GUILCHER Camille [email protected]
LOBE Cindy [email protected]
LUBRANO DI RICO Martina [email protected]
MA Feng [email protected]
MAMELLE Elisabeth [email protected]
MAREK Veronika CIFRE [email protected]
MASMOUDI Hicham [email protected]
MEJECASE Cécile [email protected]
MOURI Sarah [email protected]
PAIN - GIABICANI Eloïse [email protected]
PAIVA Solenne [email protected]
PERRA Lea [email protected]
PHAM Thi Minh Tam [email protected]
POSTAL Barbara [email protected]
PRAMIL Elodie [email protected]
RAHHAL Amer [email protected]
RIBAULT Alexandre [email protected]
RUSSICK Jules [email protected]
SALAMEH Sacha [email protected]
SANCHEZ Manuel [email protected]
SOYSOUVANH Fréderic [email protected]
TABIBZADEH Nathalie tabnahid]@gmail.com
TCHOUKAEV Anastasia [email protected]
TIAN Lei [email protected]
TOUHAMI Sara [email protected]
TRAN Sophie [email protected]
URRUTIA Alexandra [email protected]
VILLEGAS VAZQUEZ Jose [email protected]
2nd YEAR PhD student
ANDROUIN Alexandre [email protected]
AYARI Sami [email protected]
BAUM David Marcel [email protected]
BEGUIER Fanny [email protected]
BENABOU Eva [email protected]
BERTAUX Audrey [email protected]
BEURIOT Adeline [email protected]
BIGNON Yohan [email protected]
BOCCARA David [email protected]
BOKHARI Adem [email protected]
BONNET Benjamin [email protected]
BOUAZIZ Mehdi [email protected]
BRUNEL Simon [email protected]
BUONAFINE Mathieu [email protected]
CANLORBE Geoffroy [email protected]
CHARLES-MESSANCE Hugo [email protected]
CLASSE Marion [email protected]
CLAUDE Olivier [email protected]
CRON Mélanie [email protected]
DAHLQVIST Géraldine [email protected]
DAJON Marion [email protected]
DEL RIO Iratxe [email protected]
DESBOIS Anne-Claire [email protected]
DEZAIRE Ambre [email protected]
DRES Martin [email protected]
EL BOUSTANY Ray [email protected]
ESTEVE Emmanuel [email protected]
GALEOTTI Caroline [email protected]
GONNET Jessica [email protected]
GREENE Malorie [email protected]
HOLLANDE Clémence [email protected]
HU Mengyue [email protected]
HUR Justine [email protected]
JAROSSAY Annaelle [email protected]
KAPLON Hélène [email protected]
KEMGANG FANKEM Astrid Donal [email protected]
LAUNOIS Claire [email protected]
LAVIGNE Jeremy [email protected]
LEBRETON Guillaume [email protected]
LEMALE Julie [email protected]
LIABOTIS-FONTUGNE Ahanasia [email protected]
LIVROZET Marine [email protected]
LOPEZ CAYUQUEO Irma Karen [email protected]
LUCAR Olivier [email protected]
MARINELLI Ludovica [email protected]
MARTIN-GALLAUSIAUX Camille [email protected]
MIKHAILOVA Anastasia [email protected]
OUHACHI Melissa [email protected]
PECKEU Laurène [email protected]
ROUILLE Thomas [email protected]
SAGET Sarah [email protected]
SBIHI Zineb [email protected]
SEISEN Thomas [email protected]
SIMONNET Emilie [email protected]
SIQUEIROS Lourdes [email protected]
STERLIN Delphine [email protected]
TORRES LAZO Victor Renato [email protected]
VALLOT Antoine [email protected]
VAN EEGHER Sandy [email protected]
ZABLOCKI Laurent [email protected]
ZAOUI Maurice [email protected]
ZHANG Xufei [email protected]
ZHOU Xianlong [email protected]
3rd YEAR PhD student
BEUTIER Héloise [email protected]
BATAILLE Aurélien [email protected]
BOITARD Solène [email protected]
BOUYGUES Anaïs [email protected]
DE SETA Daniele [email protected]
DELIGNAT Sandrine [email protected]
EYMARD Florent [email protected]
FADLALLAH Jehane [email protected]
FLOREZ CORREDOR Laura Maria [email protected]
GALL Julie [email protected]
GEA-MALLORQUI Ester [email protected]
GENSER Laurent [email protected]
GEORGE Caroline [email protected]
GRANJON David [email protected]
HAMMOUDI Nadjib [email protected]
HANBOUCH Linda [email protected]
HANOUNA Guillaume [email protected]
HIRSCH Pierre [email protected]
ING Mathieu [email protected]
JAILLET Cyprien [email protected]
JEZIOROWSKA Dorota [email protected]
LANDMAN Cécilia [email protected]
LE MOIGNIC Aline [email protected]
LEVIN Clément [email protected]
LI Wu Zhi [email protected]
LIU Jin [email protected]
LIU Yuanhui [email protected]
LOEUILLARD Emilien [email protected]
LOISEAU Camille [email protected]
LUNELLI Luca [email protected]
LUQUE Yosu [email protected]
MASSARWEH Ahmad [email protected]
MESDOM Pierre [email protected]
MICELLI-LUPINACCI Renato [email protected]
MONSEL Antoine [email protected]
MONTASSAR Fadoua [email protected]
MUNTEANU Mona [email protected]
NABULSI QOSSQOSSI Maisa [email protected]
NEFLA Meriam [email protected]
NICOLAS Anthony [email protected]
QUENTIN Emily [email protected]
QUINIOU Valentin [email protected]
RAGOT Hélène [email protected]
RENARD PENNA Raphaele [email protected]
ROCHEFORT Juliette [email protected]
RONIN Emilie [email protected]
ROSENBAUM David [email protected]
ROUERS Angeline [email protected]
SALEM Joe-Elie [email protected]
SCHMITT Charlotte [email protected]
SERBIN Bettina [email protected]
SONNEVILLE Florence [email protected]
SOUSSI Hedi [email protected]
STEPHEN-VICTOR Emmanuel [email protected]
TANNOUS Cynthia [email protected]
TOUCH Sothea [email protected]
The Organizing Committee
Cécile BANDET
Marion DAJON
Ray EL BOUSTANY
Sarah GHEZZAL
Annaelle JAROSSAY
Hélène KAPLON
Barbara POSTAL
Elodie PRAMIL
Sami AYARI
Jules RUSSICK