Complement Factor H Deficiency Accelerates Development of Lupus Nephritis
Complement Factor H Deficiency Accelerates Development of Lupus Nephritis
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DOI：
10.1681/asn.2010060647
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发表时间：
2011-02-01
影响因子：
13.6
通讯作者：
Quigg, Richard J.
中科院分区：
文献类型：
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作者：
Bao, Lihua;Haas, Mark;Quigg, Richard J.
补体因子 H (CfH) 是旁路途径的关键调节因子，其存在于小鼠血小板和足细胞上，可以处理免疫复合物。由于免疫复合物在狼疮性肾炎病理生理学中的作用，我们研究了 CfH 在狼疮动物模型 MRL-lpr 小鼠肾炎发展中的作用。 12 周时，CfH 缺陷的 MRL-lpr 小鼠比 MRL-lpr 对照小鼠的蛋白尿和 BUN 水平明显更高。 Cfh 缺陷的 MRL-lpr 小鼠也经历了较早的死亡：在 14 周时，9 只 CfH 缺陷的 MRL-lpr 小鼠中有 6 只死于肾衰竭，而所有 11 只同窝 CfH 充足的 MRL-lpr 小鼠均存活（P
Complement factor H (CfH) is a key regulator of the alternative pathway, and its presence on mouse platelets and podocytes allows the processing of immune complexes. Because of the role of immune complexes in the pathophysiology of lupus nephritis, we studied the role of CfH in the development of nephritis in MRL-lpr mice, an animal model of lupus. At 12 weeks, CfH-deficient MRL-lpr mice had significantly more albuminuria and higher BUN levels than MRL-lpr controls. Cfh-deficient MRL-lpr mice also experienced earlier mortality: at 14 weeks, 6 of 9 CfH-deficient MRL-lpr mice had died of renal failure, whereas all 11 littermate CfH-sufficient MRL-lpr mice were alive (P