S Y Park, S Ueda, H Ohno, Y Hamano, M Tanaka, T Shiratori, T Yamazaki, H Arase, N Arase, A Karasawa, S Sato, B Ledermann, Y Kondo, K Okumura, C Ra, T Saito
J Clin Invest.
1998;
102(6):1229–1238
doi:10.1172/JCI3256
This article Copyright © 1998, The American Society for Clinical Investigation
Abstract
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mmune complex-mediated inflammation is a common mechanism of various autoimmune diseases. Glomerulonephritis (GN) is one of these diseases, and the main mechanism of the induction of GN has been unclear. We examined the contribution of Fc receptors in the induction of nephrotoxic GN by establishing and analyzing mice deficient in the Fc receptor gamma chain (FcRgamma). Whereas all wild-type mice died from severe glomerulonephritis with hypernitremia by administration of anti-glomerular basement membrane (GBM) antibodies, all FcRgamma-deficient mice survived. Histologically, wild-type mice showed glomerular hypercellularity and thrombotic changes, whereas the renal tissue in FcRgamma-deficient mice was almost intact. Deposition of anti-GBM antibody as well as complement components in the GBM were equally observed in both wild-type and knockout mice. These results demonstrate that the triggering of this type of glomerulonephritis is completely dependent on FcR+ cells.
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