Batteux F, Tourneur L, Trebeden H, Charreire J, Chiocchia G
Institut National de la Santé et de la Recherche Médicale, Unité 477, Université René Descartes, Paris, France.
J Immunol. 1999 Jan 1;162(1):603-8.
Fas-Fas ligand (FasL) interaction is required for the maintenance of immune homeostasis and seems to be responsible for the privileged immune status of some tissues. Experimental autoimmune thyroiditis (EAT), which is characterized by autoreactive T and B cell responses and a marked lymphocytic infiltration of the thyroid, is a model of choice to study the therapeutic effects of FasL. Here, we provide evidence that direct injection of DNA expression vectors encoding FasL into the inflamed thyroid inhibited development of lymphocytic infiltration of the thyroid and induced death of infiltrating T cells. These results were paralleled by a total abrogation of anti-Tg cytotoxic T cell response in FasL-treated animals vs controls. In summary, our results show that FasL expression on thyrocytes may have a curative effect on ongoing EAT by inducing death of pathogenic autoreactive infiltrating T lymphocytes.
Fas与Fas配体(FasL)的相互作用对于维持免疫稳态是必需的,并且似乎是某些组织具有免疫特权状态的原因。实验性自身免疫性甲状腺炎(EAT)以自身反应性T和B细胞反应以及甲状腺明显的淋巴细胞浸润为特征,是研究FasL治疗效果的理想模型。在此,我们提供证据表明,将编码FasL的DNA表达载体直接注射到发炎的甲状腺中可抑制甲状腺淋巴细胞浸润的发展,并诱导浸润性T细胞死亡。与对照组相比,FasL处理的动物中抗Tg细胞毒性T细胞反应完全消除,这些结果与之相符。总之,我们的结果表明,甲状腺细胞上的FasL表达可能通过诱导致病性自身反应性浸润T淋巴细胞死亡,对正在进行的EAT产生治疗作用。