间质性肾炎中的抗独特型免疫。II. 患抗肾小管基底膜病的大鼠无法产生抗独特型调节反应：RT7.1 +、OX8 - 抑制性T细胞机制的调节作用。
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.
作者信息
Neilson E G, McCafferty E, Phillips S M, Clayman M D, Kelly C J
出版信息
J Exp Med. 1984 Apr 1;159(4):1009-26. doi: 10.1084/jem.159.4.1009.
Abstract
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.
摘要
抗独特型免疫能够成功抑制导致间质性肾炎的抗肾小管基底膜（αTBM）疾病的发展。然而，正常免疫以引发疾病的大鼠并不会产生这种调节性和保护性的抗独特型效应。未能观察到这种调节性反应在功能上与免疫后不久出现的非特异性RT7.1+、OX8抑制性T细胞的影响有关。虽然这种抑制性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，并且据推测，会使疾病进程处于可操作的活跃模式。
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