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IgE causes immediate (type I) hypersensitivities› Characterized by immediate reaction of the
sensitized individual Generally within minutes of exposure
Tendency to have type I hypersensitivities is inherited› Reactions occur in at least 20% to 30% of
population
Sensitization occurs when antigen makes contact with some part of body and induces response
IgE antibodies bind to receptors on mast cells and basophiles› Antigen readily bonds to cells fixed with IgE
antibodies Within seconds, mast cells degranulate releasing
mediators that initiate immune reaction including hives, hay fever and anaphylaxis
Localized anaphylaxis› Most allergic reactions are local
anaphylaxis Hives
Allergic skin condition characterized by formation of wheal and flare rash
Hay fever Allergic condition caused by inhaled
antigen Condition marked by itching teary eyes,
sneezing and runny nose Asthma
Respiratory allergy Allergic mediators attracted to inflamed
respiratory tract Results in increased mucous
secretion and bronchi spasm
Generalized anaphylaxis› Rare, but more serious› Antigen enters bloodstream and becomes
widespread Reactions affect almost entire body Can induce shock
› Massive release of mediators causes extensive blood vessel dilation and fluid loss Causes fall in pressure leading to blood flow
insufficiency
Immunotherapy› General term for
techniques used to modify immune system for favorable effect
› Procedure is to inject individual with extremely dilute suspension of allergen Called desensitization or
hyposensitization› Concentration of
allergen gradually increased over time Individual gradually
becomes less sensitive
Immunotherapy› Second therapeutic procedure is injection
of antibodies to bind IgE Essentially anti-IgE antibodies
› Most IgE are bound to mast cells and basophiles
Engineered anti-IgE created rhuMab = recombinant human Monoclonal antibody
Complement-fixing antibodies react with cell surface antigens causing cell injury or death
Cells can be destroyed in type II reactions through complement fixation and antibody-dependent cellular cytotoxicity (ADCC)
Examples of type II hypersensitivities are› Transfusion reactions› Hemolytic disease of the newborn
Transfusion reactions› Normal red blood cells have different surface
antigens Antigens differ from person to person
People are designated type A, B, AB or O
› Transfused blood that is antigenically different can be lysed by recipient immune cells
› Cross-matching blood is used to ensure compatibility between donor and recipient
› Antibody-coated cells removed by phagocyte system
› Symptoms include low blood pressure, pain, nausea and vomiting
Hemolytic disease of the newborn› Basis of disease is incompatibility of Rh
factor between mother and child Rh factor RBC cell surface antigen
Rh positive = Rh antigen present Rh negative = Rh antigen missing
Anti-Rh antibodies form in Rh negative mother pregnant with Rh positive fetus First Rh positive fetus unharmed Second Rh positive fetus provokes
strong secondary immune response IgG antibodies of secondary
response cross placenta causing extensive damage to fetal red blood cells
Immune complexes consist of antigen and antibody bound together
Usually adhere to Fc receptors on cells› Complexes are destroyed and removed
Certain instances complexes persist in circulation or at sites of formation› Initiate blood clotting mechanism› Activate complement contributing to inflammation
Complexes commonly deposited in skin, joints and kidney
Complexes also cause disseminated intravascular coagulation (DIC)› Clots in small vessels
Leads to system failure
Delayed hypersensitivities caused by cell-mediated immunity› Slowly developing response to antigen
Reactions peak in 2 to 3 days instead of minutes
T cells are responsible for reactions› Reactions can occur nearly anywhere in the
body Delayed hypersensitivity reactions
responsible for contact dermatitis, tissue damage, rejection of tissue grafts and some autoimmune diseases
Tuberculin skin test› Test involves
introduction of small quantities of protein antigens from tubercle bacillus into skin
› In positive skin test injection site reddens and gradually thickens Reaction reaches peak
in 2 to 3 days
› Reactions result from sensitized T cells, release of cytokines and influx of macrophages
Contact hypersensitivities› Mediated by the T cells
T cells release cytokines Cytokines initiate inflammation
that attracts macrophages Macrophages release
mediators to add to inflammation
› Common examples of contact allergies include Poison ivy and poison oak Nickel in metal jewelry Chromium salts in leather Latex products
Major drawback to graft transplantation is possible immunological rejection› Differences between donor and recipient tissues basis
for rejection› Rejection is predominantly type IV reaction
Killing of graft cells occurs through complex combination of mechanisms› Contact with sensitized cytotoxic T cells and natural
killer cells Combination of agents commonly used to
prevent graft rejection› Cyclosporin A› Steroids› Basiliximab
Monoclonal antibody preparation Blocks binding of immune mediators
Body usually recognizes self antigens› Destroys lymphocytes that would destroy self› Malfunction in immune recognition basis for
autoimmunity Autoimmune diseases may result from reactions
to antigens that are similar to self antigens Autoimmunity may occur after tissue injury
› Self antigens released from injured organ Autoantibodies form and interact with injured tissues and
cause further damage
Spectrum of autoimmune diseases› Reactions occur over spectrum
Organ-specific to widespread responses› Organ-specific
Thyroid disease Only thyroid is affected
› Widespread response Lupus
Autoantibodies made against nuclear constituents of all body cells
Rheumatoid arthritis Immune response made against collagen in
connective tissue Myasthenia gravis
Autoantibody-mediated disease Antibody to acetylcholine receptor proteins
Treatment of autoimmune diseases› Treatment aimed at:
Killing dividing cells Immunosuppressant
Controlling T cell signaling Cyclosporin
Anti-inflammatory medications Cortisone-like steroids
Replacement therapy Insulin
Immunodeficiency disorders are marked by the body’s inability to make and sustain an adequate immune response
Two basic types of disorders› Primary or congenital
Inborn as a result of genetic defect or developmental abnormality
› Secondary or acquired Can be acquired as result of infection or
other stressor
Primary immunodeficiencies› Generally rare› Examples
Agammaglobulinemia Few or no antibodies produced Occurs in 1 in 50,000 people
Severe combined immunodeficiency disorder (SCID) Neither B nor T lymphocytes are functional Occurs in 1 in 500,000 live births
Selective IgA deficiency Little or no IgA produced Most common disorder
One in 333 to 700 people
Secondary immunodeficiencies› Result from environmental, rather than genetic
factors Malignancies, advanced age certain infections,
immunosuppressive drugs and malnutrition are just a few
› Often results from depletion of certain cells of the immune system Syphilis, leprosy and malaria affect T-cell population and
macrophage function Malignancies of lymphoid system decrease antibody-
mediated immunity
› Most serious widespread immunodeficiency is AIDS Destroys helper T cells
Inhibits initiation of cellular and antibody-mediated immunity