首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Antiidiotypic immunity in interstitial nephritis. II. Rats developing anti-tubular basement membrane disease fail to make an antiidiotypic regulatory response: the modulatory role of an RT7.1+ OX8- suppressor T cell mechanism
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Antiidiotypic immunity in interstitial nephritis. II. Rats developing anti-tubular basement membrane disease fail to make an antiidiotypic regulatory response: the modulatory role of an RT7.1+ OX8- suppressor T cell mechanism

机译:间质性肾炎的抗独特型免疫。二。发生抗肾小管基底膜疾病的大鼠无法做出抗独特型调节反应:RT7.1 +OX8-抑制性T细胞机制的调节作用

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摘要

Antiidiotypic immunity can successfully inhibit the development of antitubular basement membrane (alpha TBM) disease that produces interstitial nephritis. Rats normally immunized to produce disease, however, do not develop this regulatory and protective antiidiotypic effect. The failure to see such a regulatory response is functionally related to the influence of a nonspecific, RT7.1+, OX8-suppressor T cell that appears shortly after immunization. While this suppressor cell system can partially reduce the intensity of disease, it also limits the host's ability to specifically regulate the alpha TBM immune response and, hypothetically, leaves the disease process in an operationally active mode.
机译:抗独特型免疫可以成功抑制产生间质性肾炎的抗肾小管基底膜(alpha TBM)疾病的发展。但是,正常免疫产生疾病的大鼠不会产生这种调节性和保护性抗独特型作用。未能看到这种调节反应在功能上与免疫后不久出现的非特异性RT7.1 + OX8抑制T细胞的影响有关。尽管这种抑制细胞系统可以部分降低疾病的强度,但它也限制了宿主特异性调节αTBM免疫反应的能力,并且假设使疾病过程处于可操作的活动模式。

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