Ware R, Jiang H, Braunstein N, Kent J, Wiener E, Pernis B, Chess L
Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York 10032.
Immunity. 1995 Feb;2(2):177-84. doi: 10.1016/s1074-7613(95)80066-2.
CD8+ T cells control immune responses, and recent studies suggest that this regulation is, in part, specifically directed towards TCR structures expressed by CD4+ cells. To develop a system to study the role of the TCR in regulatory interactions, we isolated clones of CD4+ cells expressing identified TCR V beta chains. These CD4+ clones were used to stimulate and expand autologous CD8+ cells, which kill the inducing CD4+ clone as well as independently isolated autologous CD4+ clones sharing the same TCR V beta as the inducing cell but not CD4+ T cells expressing different V beta TCRs. This V beta-specific cytotoxicity is dependent on the state of activation of the target cells and is not inhibited by an anti-class I monoclonal antibody, W6/32. We envision that V beta-specific CD8+ T cells of this type may regulate immune responses by direct interaction with antigen-activated CD4+ cells.
CD8 + T细胞控制免疫反应,最近的研究表明,这种调节部分是专门针对CD4 +细胞所表达的TCR结构的。为了开发一个系统来研究TCR在调节相互作用中的作用,我们分离了表达已鉴定TCR Vβ链的CD4 +细胞克隆。这些CD4 +克隆用于刺激和扩增自体CD8 +细胞,后者会杀死诱导性CD4 +克隆以及独立分离的与诱导细胞共享相同TCR Vβ但不表达不同VβTCR的自体CD4 +克隆。这种Vβ特异性细胞毒性取决于靶细胞的激活状态,并且不受抗I类单克隆抗体W6/32的抑制。我们设想,这种类型的Vβ特异性CD8 + T细胞可能通过与抗原激活的CD4 +细胞直接相互作用来调节免疫反应。