Lu P, Wang Y L, Linsley P S
Department of Immunomodulation, Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121, USA.
Curr Opin Immunol. 1997 Dec;9(6):858-62. doi: 10.1016/s0952-7915(97)80190-2.
Antigen presentation by CD80/CD86-positive 'professional APCs' induces T-cell activation, whereas antigen presentation in the absence of sufficient CD80/CD86 costimulation may induce a form of tolerance. Blocking CD80/CD86 constimulation inhibits autoimmune disease progression in a variety of animal models, but whether these effects result from restoration of self-tolerance or temporary disease blockade is still unclear. The individual roles of CD80 and CD86 in autoimmune diseases are complicated by multiple factors in vivo. Data from B7 gene knockout mice further clarify the importance of CD80/CD86 in the regulation of T-cell activation and tolerance.
由CD80/CD86阳性的“专职抗原呈递细胞”进行的抗原呈递可诱导T细胞活化,而在缺乏足够CD80/CD86共刺激的情况下进行抗原呈递可能会诱导一种耐受形式。在多种动物模型中,阻断CD80/CD86共刺激可抑制自身免疫性疾病的进展,但这些效应是源于自身耐受的恢复还是疾病的暂时阻断仍不清楚。CD80和CD86在自身免疫性疾病中的个体作用因体内多种因素而变得复杂。来自B7基因敲除小鼠的数据进一步阐明了CD80/CD86在调节T细胞活化和耐受中的重要性。