@article{oai:niigata-u.repo.nii.ac.jp:00016035, author = {山本, 格}, issue = {5}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {May}, note = {A prototype of anti-glomerular basement membrane (GBM):nephritis is induced by administrating rabbit anti-rat GBM antibody in rats. Glomerulonerphritis occurs within minutes after binding of the antibody to GBM, followed by fixation of complement and accumulation of polymorphonuclear leukocytes and monocytes/macrophages. In contrast to the prototype of anti-GBM nephritis, a novel type was evoked a few days after anti-GBM antibody of smaller dose was given in Wistar Kyoto (WKY) rats. The model is characterized by glomerular accumulation of CD 8-positive lymphocytes and monocytes/macrophages, crescent formation and critical renal insufficiency. Lnterestingly the anti-GBM nephritis is almost completely suppressed in CD 8-positive lymphocyte-depleted WKY rats, indicating a crucial role of. the lymphoocytes in the induction. The glomerular accumulation of CD 8-positive lymphocytes and monocytes/macrophages is mediated by ICAM-1-B 1 integrin interaction and chemokines such as MCP-1. The CD 8-positive lymphocytes express a B T cell receptor and perforin/granzyme B, indicating that they are cytotoxic T cells and injure glomerular cells through release of perforin/granzyme B. These results strongly suggest that cellular immunity is involved in mediation of the novel anti-GBM nephritis model in WKY rats even though anti-GBM antibody is the trigger. A possible involvement of cellular immunity in human glomerulonephritis should be examined in the future.}, pages = {237--242}, title = {1)抗基底膜型糸球体腎炎の新しいモデル(シンポジウム 糸球体腎炎をめぐる最近の話題, 第539回新潟医学会)}, volume = {113}, year = {1999} }