Susceptibility of mast cell-deficient W/Wv mice to pristane-induced experimental lupus nephritis
Susceptibility of mast cell-deficient W/Wv mice to pristane-induced experimental lupus nephritis
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DOI：
10.1016/j.imlet.2003.11.014
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发表时间：
2004-02-15
影响因子：
4.4
通讯作者：
Peng, SL
中科院分区：
文献类型：
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作者：
Lin, L;Gerth, AJ;Peng, SL
在许多器官特异性自身免疫性疾病模型中，肥大细胞在自身抗体和终末器官炎症之间提供了关键的细胞联系，从而引发和传播疾病。然而，它们在系统性自身免疫中的作用仍然是推测性的。因此，我们研究了肥大细胞在系统性免疫复合物相关自身免疫性疾病（狼疮性肾炎）的小鼠模型中的作用，期望观察在没有终末器官疾病的情况下体液自身免疫的发展。令人惊讶的是，肥大细胞缺陷的动物不仅会出现狼疮的特征性体液特征，包括高丙种球蛋白血症和自身抗体，而且还会出现免疫复合物肾小球肾炎，如肾脏免疫沉积、肾小球疾病和蛋白尿所证明的那样。这些发现表明，在不道德自身免疫性疾病中存在不同的终末器官损伤效应途径：一种涉及自身抗体和肥大细胞之间的相互作用，以在器官特异性自身免疫中招募炎症，另一种涉及全身自身免疫中自身抗体与循环炎症介质之间更直接的、不依赖于肥大细胞的相互作用。 (C) 2003 Elsevier B.V. 保留所有权利。
In many models of organ-specific autoimmune diseases, mast cells provide a critical cellular link between autoantibodies and end-organ inflammation, both initiating and propagating disease. However, their role in systemic autoimmunity remains speculative. We therefore examined the role of mast cells in a murine model of systemic immune complex-related autoimmune disease, lupus nephritis, expecting to observe the development of humoral autoimmunity in the absence of end-organ disease. Surprisingly, not only did mast cell-deficient animals develop characteristic humoral features of lupus, including hypergammaglobulinemia and autoantibodies, they also developed immune complex glomerulonephritis, as evidenced by renal immune deposits, glomerular disease, and proteinuria. These findings implicate the presence of distinct effector pathways to end-organ damage in Immoral autoimmune diseases: one involving the interaction between autoantibodies and mast cells to recruit inflammation in organ-specific autoimmunity, and another involving a more direct-mast cell-independent-interaction between autoantibodies and circulating inflammatory mediators in systemic autoimmunity. (C) 2003 Elsevier B.V. All rights reserved.