Karandikar N J, Vanderlugt C L, Bluestone J A, Miller S D
Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Northwestern University Medical School, Chicago, IL 60611, USA.
J Neuroimmunol. 1998 Aug 14;89(1-2):10-8. doi: 10.1016/s0165-5728(98)00058-7.
The B7/CD28:CTLA-4 costimulatory pathway plays a critical role in determining the fate of immune responses (activation vs. down-regulation) and is a highly promising therapeutic target for treating autoimmune diseases. In this review, we highlight the mechanisms by which this costimulatory pathway operates emphasizing the role of the different components in the pathogenesis of relapsing experimental autoimmune encephalomyelitis, a CD4 T cell-mediated autoimmune model of multiple sclerosis. The separate and distinct roles of B7-1, B7-2 and CTLA-4 in positive and negative regulation of autoimmune pathogenesis are considered and a working model is proposed.
B7/CD28:CTLA-4共刺激通路在决定免疫反应的命运（激活与下调）中起关键作用，是治疗自身免疫性疾病极具前景的治疗靶点。在本综述中，我们着重介绍了该共刺激通路的作用机制，强调了不同组分在复发型实验性自身免疫性脑脊髓炎（一种CD4 T细胞介导的多发性硬化自身免疫模型）发病机制中的作用。我们考虑了B7-1、B7-2和CTLA-4在自身免疫发病机制的正向和负向调节中各自独特的作用，并提出了一个工作模型。
