Vella A T, McCormack J E, Linsley P S, Kappler J W, Marrack P
Howard Hughes Medical Institute, Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
Immunity. 1995 Mar;2(3):261-70. doi: 10.1016/1074-7613(95)90050-0.
In mice injected with superantigens, T cells specific for that antigen proliferate and then die. It has been suggested that the target cells die because they encounter superantigen on the surfaces of nonprofessional presenting cells, such as B cells, which cannot deliver costimulatory signals to T cells. A number of reagents that induce costimulatory molecules on B cells were tested. Lipopolysaccharide very effectively prevented T cell death driven by superantigen. Perhaps surprisingly, the action of lipopolysaccharide was not mediated through the expected costimulatory molecule, B7. Rather, the effects of lipopolysaccharide involved the production of inflammatory cytokines, in particular TNF alpha. The rescued cells survived in vitro culture and were resistant to Fas-induced killing. These data demonstrate that LPS can block antigen-induced T cell death perhaps by interfering with Fas signaling.
在注射了超抗原的小鼠中，针对该抗原的特异性T细胞会增殖然后死亡。有人提出，靶细胞死亡是因为它们在非专职呈递细胞（如B细胞）的表面遇到了超抗原，而这些细胞无法向T细胞传递共刺激信号。人们测试了多种能诱导B细胞上共刺激分子的试剂。脂多糖非常有效地阻止了由超抗原驱动的T细胞死亡。也许令人惊讶的是，脂多糖的作用并非通过预期的共刺激分子B7介导。相反，脂多糖的作用涉及炎症细胞因子的产生，特别是肿瘤坏死因子α。被挽救的细胞在体外培养中存活下来，并且对Fas诱导的杀伤具有抗性。这些数据表明，脂多糖可能通过干扰Fas信号传导来阻断抗原诱导的T细胞死亡。
