Resistance of Fc receptor-deficient mice to fatal glomerulonephritis
Resistance of Fc receptor-deficient mice to fatal glomerulonephritis
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DOI：
10.1172/jci3256
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发表时间：
1998-09-15
影响因子：
15.9
通讯作者：
Saito, T
中科院分区：
文献类型：
--
作者：
Park, SY;Ueda, S;Saito, T
免疫复合物介导的炎症是各种自身免疫性疾病的共同机制。肾小球肾炎（GN）就是其中之一，其发病机制尚不清楚。我们通过建立和分析Fc受体γ链（FcR γ）缺陷的小鼠，研究了Fc受体在诱导肾毒性GN中的作用。而所有野生型小鼠死于严重的肾小球肾炎与高氮血症的管理抗肾小球基底膜（GBM）抗体，所有FcR γ缺陷小鼠存活。在组织学上，野生型小鼠表现出肾小球细胞过多和血栓形成的变化，而FcR γ缺陷小鼠的肾组织几乎是完整的。在野生型和基因敲除小鼠中同样观察到抗GBM抗体以及补体成分在GEM中的沉积。这些结果表明，触发这种类型的肾小球肾炎是完全依赖于FcR（+）细胞。
Immune 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 (FcR gamma). Whereas all wild-type mice died from severe glomerulonephritis with hypernitremia by administration of anti-glomerular basement membrane (GBM) antibodies, all FcR gamma-deficient mice survived. Histologically, wild-type mice showed glomerular hypercellularity and thrombotic changes, whereas the renal tissue in FcR gamma-deficient mice was almost intact. Deposition of anti-GBM antibody as well as complement components in the GEM 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.