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能特异性清除表达Vβ8 TCR的自体CD4 + T细胞的小鼠CD8 + T细胞:Qa-1分子的作用

Murine CD8+ T cells that specifically delete autologous CD4+ T cells expressing V beta 8 TCR: a role of the Qa-1 molecule.

作者信息

Jiang H, Ware R, Stall A, Flaherty L, Chess L, Pernis B

机构信息

Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032.

出版信息

Immunity. 1995 Feb;2(2):185-94. doi: 10.1016/s1074-7613(95)80079-4.

Abstract

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.

摘要

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。

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