Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat I. A role for T suppressor cells
Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat I. A role for T suppressor cells
复制标题
挪威布朗大鼠氯化汞肾炎自身抗体合成的自身调节 I. T 抑制细胞的作用
DOI：
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发表时间：
1984
影响因子：
5.4
通讯作者：
C. Lockwood
中科院分区：
文献类型：
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作者：
C. Bowman;D. Mason;C. Pusey;C. Lockwood
在Brown Norway大鼠中注射氯化汞可诱导抗肾小球基底膜（GBM）自身抗体的瞬时形成。在循环中的抗GBM自身抗体不再可检测到后，从恢复期动物转移脾细胞，可抑制HgCl 2在幼稚受体中的疾病再诱导。当T抑制细胞群在转移前被单克隆抗体MRCOX8耗尽时，这种抑制作用显著降低。我们的研究表明T抑制细胞在自身免疫性肾炎动物模型中的自身调节作用，并可能为人类抗GBM疾病的特异性治疗设计奠定基础。
Mercuric chloride injections in the Brown Norway rat induce the transient formation of anti‐glomerular basement membrane (GBM) autoantibodies. Transfer of spleen cells from convalescent animals, after circulating anti‐GBM autoantibodies are no longer detectable, inhibits reinduction of the disease by HgCl2 in naive recipients. This inhibition is significantly less when the T suppressor cell population is depleted by the monoclonal antibody, MRCOX8, before transfer. Our studies suggest a role for T suppressor cells in autoregulation in this animal model of autoimmune nephritis and may form a basis for the design of specific therapy for anti‐GBM disease in man.