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2004 | 52 | 2 | 96-103
Article title

Anti-GBM glomerulonephritis: a T cell-mediated autoimmune disease?

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Abstracts
EN
Anti-glomerular basement membrane (GBM) glomerulonephritis, which was among the earliest recognized human autoimmune diseases, is characterized by the presence of anti- -GBM antibody. It has been a prototypical example of autoantibody-mediated autoimmune disease. However, decades of research on this disease, based either on clinical observations or experimental models, have revealed that T cell-mediated cellular immunity may potentially be a more important mediator of glomerulonephritis. We have made several breakthroughs in understanding the T cell-mediated mechanism causing this disease in a rat model based on Goodpasture's antigen, non-collagen domain 1 of ?3 chain of type IV collagen (Col4alpha3NC1). We demonstrated that anti-GBM glomerulonephritis was induced by either passive transfer of Col4alpah3NC1-specific T cells or active immunization with the nephritogenic T cell epitope of Col4alpha3NC1. Immunization with the T cell epitope also triggered production of anti-GBM antibodies to diversified GBM antigens. Thus, a single nephritogenic T cell epitope alone is sufficient to induce the clinical spectrum of anti-GBM glomerulonephritis, including proteinuria, glomerular injury, and anti-GBM antibody. A possible T cell-mediated mechanism for causing human anti-GBM disease is proposed.
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Year
Volume
52
Issue
2
Pages
96-103
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author
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ARTICLE
Publication order reference
Ya-Huan Lou, Department of Diagnostic Science, Dental Branch, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
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YADDA identifier
bwmeta1.element.element-from-psjc-441e8fb9-69a1-3ee0-9d0b-a6b0d2932258
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