Mann R, Neilson E G
J Immunol. 1986 Feb 1;136(3):908-12.
We observed the emergence of an antigen-specific Lyt-2+ suppressor T cell after the i.v. injection of tubular antigen-derivatized lymphocytes into mice already immunized to produce interstitial nephritis. The auto-induction of these suppressor T cells effectively attenuated both the expression of renal injury and a delayed-type hypersensitivity response to tubular antigen. This suppressive effect was also genetically restricted by gene products in I-J and Igh-1. Although this suppressor system had a marked inhibitory effect on the nephritogenic effector cell repertoire, there was no diminution of titers of antibodies to the tubular basement membrane. Our results demonstrate a protective role for antigen-specific suppressor cells in autoimmune renal injury, and the strategy for their induction may have important therapeutic implications for other immune-mediated disorders.
我们观察到,在已免疫产生间质性肾炎的小鼠静脉注射肾小管抗原衍生淋巴细胞后,出现了抗原特异性Lyt-2⁺抑制性T细胞。这些抑制性T细胞的自身诱导有效地减轻了肾损伤的表达以及对肾小管抗原的迟发型超敏反应。这种抑制作用也受到I-J和Igh-1基因产物的遗传限制。尽管该抑制系统对致肾炎效应细胞库有显著的抑制作用,但针对肾小管基底膜的抗体滴度并未降低。我们的结果证明了抗原特异性抑制细胞在自身免疫性肾损伤中的保护作用,其诱导策略可能对其他免疫介导的疾病具有重要的治疗意义。