Jiang H, Ware R, Stall A, Flaherty L, Chess L, Pernis B
Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032.
Immunity. 1995 Feb;2(2):185-94. doi: 10.1016/s1074-7613(95)80079-4.
Interactions mediated by TCRs expressed on different T cell subsets may play a role in immunoregulation. To investigate this idea, we studied the regulation of superantigen-induced TCR V beta-restricted responses. We asked whether the in vivo regulation of CD4+ V beta 8+ T cells following SEB injection is controlled by CD8+ T cells. We found that in mice deficient in CD8+ T cells, the down-regulation of CD4+ V beta 8+ T cells below baseline is not observed. Moreover, following SEB administration, CD8+ T cells emerge that preferentially kill subpopulations of activated CD4+ V beta 8+ but not CD4+ V beta 8- T cells in vitro. This TCR V beta-specific cytotoxicity is dependent on beta 2-microglobulin and is inhibited by antisera specific for Qa-1 but not by antibody to MHC class Ia. These data suggest the idea that the specificity of immune regulation may involve CD8+ T cell recognition of TCR V beta determinants and Qa-1 molecules expressed on CD4+ T cells.
表达于不同T细胞亚群上的TCR介导的相互作用可能在免疫调节中发挥作用。为了探究这一观点，我们研究了超抗原诱导的TCR Vβ限制性应答的调节。我们询问注射SEB后CD4+ Vβ8+ T细胞在体内的调节是否受CD8+ T细胞控制。我们发现，在缺乏CD8+ T细胞的小鼠中，未观察到CD4+ Vβ8+ T细胞下调至基线以下。此外，注射SEB后，出现了CD8+ T细胞，其在体外优先杀伤活化的CD4+ Vβ8+ 亚群而非CD4+ Vβ8- T细胞。这种TCR Vβ特异性细胞毒性依赖于β2-微球蛋白，并被针对Qa-1的抗血清抑制，但不被MHC I类抗体抑制。这些数据表明，免疫调节的特异性可能涉及CD8+ T细胞对CD4+ T细胞上表达的TCR Vβ决定簇和Qa-1分子的识别。
