Wakashin Y, Ueda S, Yoshida H, Mori T, Mori Y, Iesato K, Ogawa M, Wakashin M
First Department of Internal Medicine, Chiba University Hospital.
Nihon Jinzo Gakkai Shi. 1992 Jun;34(6):657-67.
Autoantibody formation and lymphocytes proliferative response to tubular basement membrane (TBM) antigen were examined to clarify the pathogenesis of gold nephropathy, in rheumatoid arthritis patients. The existence of tubulopathy was ascertained by urine protein analysis, electrophoresis and urine TBM antigen titration. Circulating antibody to human TBM antigen titrated by enzyme immunoassay was significantly elevated in patients with gold tubulopathy, and mitogenic stimulation with TBM antigen of peripheral lymphocytes specifically responded in the early stage after receiving gold, but then clearly decreased after the cessation of gold. But, when the lymphocytes had been passed through a nylon wool column, the reaction was remarkably high even in the later stage after receiving gold, suggesting that another suppressive population of lymphocytes became trapped in the nylon wool column. This evidence suggests that gold compounds definitely act as initiating and promoting agents, and the development of tubular disorders induced by gold are likely related to the cellular recognition of effector T cells to the TBM antigen, following the strong effect of gold on the cellular immune system.
为了阐明类风湿关节炎患者金肾病的发病机制，对自身抗体形成以及淋巴细胞对肾小管基底膜（TBM）抗原的增殖反应进行了检测。通过尿蛋白分析、电泳和尿TBM抗原滴定确定肾小管病变的存在。用酶免疫测定法滴定的针对人TBM抗原的循环抗体在金诱导的肾小管病变患者中显著升高，并且外周淋巴细胞对TBM抗原的促有丝分裂刺激在接受金治疗后的早期有特异性反应，但在停止金治疗后明显下降。但是，当淋巴细胞通过尼龙毛柱时，即使在接受金治疗后的后期反应也非常高，这表明另一群抑制性淋巴细胞被困在了尼龙毛柱中。这一证据表明金化合物肯定起到了启动和促进作用，并且金诱导的肾小管疾病的发展可能与金对细胞免疫系统产生强烈影响后效应T细胞对TBM抗原的细胞识别有关。
