用抗I-A单克隆抗体治疗（新西兰黑鼠×新西兰白鼠）F1代疾病。
Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies.
作者信息
Adelman N E, Watling D L, McDevitt H O
出版信息
J Exp Med. 1983 Oct 1;158(4):1350-5. doi: 10.1084/jem.158.4.1350.
Abstract
(NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals produced a remission in female mice with established renal disease. The results demonstrated that anti-I-A therapy stabilized the level of proteinuria and increased the 1-yr survival rate from 10% to greater than 90% in treated animals relative to control mice. These findings may ultimately have therapeutic potential for the treatment of systemic lupus erythematosus.
摘要
（新西兰黑鼠×新西兰白鼠）F1代小鼠会自发形成一种自身免疫综合征，其特征为致命性免疫复合物肾小球肾炎。给予针对与这些动物肾小球肾炎易感性相关的H-2单倍型I区基因产物（I-Az）的单克隆抗体，可使患有已确诊肾病的雌性小鼠病情缓解。结果表明，相对于对照小鼠，抗I-A治疗可稳定蛋白尿水平，并使治疗动物的1年生存率从10%提高至90%以上。这些发现最终可能对系统性红斑狼疮的治疗具有潜在的治疗价值。
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Mechanisms of regulation of cell-mediated immunity: anti-I-A alloantisera interfere with induction and expression of T-cell-mediated immunity to cell-bound antigen in vivo.细胞介导免疫的调节机制：抗I-A同种异体抗血清在体内干扰对细胞结合抗原的T细胞介导免疫的诱导和表达。
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