+ All Categories
Home > Documents > About the cover illustration

About the cover illustration

Date post: 01-Jan-2017
Category:
Upload: phungtram
View: 214 times
Download: 1 times
Share this document with a friend
1
About the cover illustration ERNEST GOODPASTURE AND GLOMERULONEPHRITIS In 1919, Ernest Goodpasture (right) described the syndrome of rapidly-progressive glomer- ulonephritis in association with pulmonary hemorrhage. Eventually, this syndrome was found to result from the production of antibodies against basement membrane, reacting both with the glomerular basement membrane and with that of alveoli. On renal biopsy, this type of glomer- ulonephritis may be recognized by the smooth, nearly linear deposition of immunoglobulin along the basement membrane. Such deposition may be nicely demonstrated by immunofluorescent staining, as shown on the left (image may be seen in color on the J Lab Clin Med website). It has been difficult to establish just what antigen is detected by the Goodpasture antibodies. They recognize the 3 noncollagenous domain of type IV collagen, and T-cell involvement in the development of glomerulitis suggests that linear peptides are important. A 36-amino-acid sequence from the carboxy terminus was thought to be the key epitope, but it cannot produce the disease by itself. An article in this month’s issue of the Journal examines overlapping peptides covering the length of the target domain, and found that none of them would reliably produce glomerulitis in an experimental model of Goodpasture’s disease. Two peptides produced mild nephritis in a minority of animals; several could provoke a T-cell mitogenic response in animals that already had the syndrome. It appears that more than one antigen is necessary to produce this type of nephritis, and/or that the antigen must undergo conformational change or port-translational modification in order to work its effect. The paper, by An-Ming Luo and colleagues, may be found on page 303. Dale E. Hammerschmidt, MD Editor-in-Chief Note: The glomerular image in the left panel is provided through the courtesy of the WebPath image base, maintained for educational and teaching use by the Pathology Department of the University of Utah. We thank Dr Edward C. Klatt of Florida State University for permission to use this image, and we commend his collection to our readers: http://www.medlib.med.utah.edu/webpath/webpath.html. J Lab Clin Med 2002;139:324. Copyright © 2002 by Mosby, Inc. 0022-2143/2002 $35.00 0 5/8/124553 doi:10.1067/mlc.2002.124553 324
Transcript

About the cover illustration

ERNEST GOODPASTURE AND GLOMERULONEPHRITIS

In 1919, Ernest Goodpasture (right) described the syndrome of rapidly-progressive glomer-ulonephritis in association with pulmonary hemorrhage. Eventually, this syndrome was found toresult from the production of antibodies against basement membrane, reacting both with theglomerular basement membrane and with that of alveoli. On renal biopsy, this type of glomer-ulonephritis may be recognized by the smooth, nearly linear deposition of immunoglobulin alongthe basement membrane. Such deposition may be nicely demonstrated by immunofluorescentstaining, as shown on the left (image may be seen in color on the J Lab Clin Med website).

It has been difficult to establish just what antigen is detected by the Goodpasture antibodies.They recognize the �3 noncollagenous domain of type IV collagen, and T-cell involvement in thedevelopment of glomerulitis suggests that linear peptides are important. A 36-amino-acid sequencefrom the carboxy terminus was thought to be the key epitope, but it cannot produce the disease byitself. An article in this month’s issue of the Journal examines overlapping peptides covering thelength of the target domain, and found that none of them would reliably produce glomerulitis inan experimental model of Goodpasture’s disease. Two peptides produced mild nephritis in aminority of animals; several could provoke a T-cell mitogenic response in animals that already hadthe syndrome. It appears that more than one antigen is necessary to produce this type of nephritis,and/or that the antigen must undergo conformational change or port-translational modification inorder to work its effect. The paper, by An-Ming Luo and colleagues, may be found on page 303.

Dale E. Hammerschmidt, MDEditor-in-Chief

Note: The glomerular image in the left panel is provided through the courtesy of the WebPath image base, maintained foreducational and teaching use by the Pathology Department of the University of Utah. We thank Dr Edward C. Klatt ofFlorida State University for permission to use this image, and we commend his collection to our readers:http://www.medlib.med.utah.edu/webpath/webpath.html.

J Lab Clin Med 2002;139:324.

Copyright © 2002 by Mosby, Inc.

0022-2143/2002 $35.00 � 0 5/8/124553

doi:10.1067/mlc.2002.124553

324

Recommended