Lederman S, Yellin M J, Krichevsky A, Belko J, Lee J J, Chess L
Department of Medicine, Columbia University, New York, New York 10032.
J Exp Med. 1992 Apr 1;175(4):1091-101. doi: 10.1084/jem.175.4.1091.
CD4+ T lymphocytes provide contact-dependent stimuli to B cells that are critical for the generation of specific antibody responses in a process termed T helper function. The surface structures on activated CD4+ T cells that mediate this function are not fully known. We previously reported the isolation of a functionally unique subclone of the Jurkat leukemic T cell line (D1.1) that constitutively expressed contact-dependent helper effector function. To identify T cell surface molecules that mediate contact-dependent T helper function, a monoclonal antibody (mAb), designated 5c8, was generated that inhibits D1.1-mediated B cell activation and immunoprecipitates a novel 30-kD protein structure from surface-iodinated D1.1 cells. Normal CD4+ T cells express 5c8 antigen (Ag) transiently 5-6 h after activation by phorbol myristate acetate and phytohemagglutinin with maximal expression 5-6 h after activation and absence of expression by 24 h. In contrast, neither resting nor activated CD8+ T cells express 5c8 Ag. In functional studies, mAb 5c8 inhibits the ability of fixed, activated CD4+ T cells to induce B cell surface CD23 expression. In addition, mAb 5c8 inhibits the ability of CD4+ T cells to direct terminal B cell differentiation driven by pokeweed mitogen. Taken together, these data suggest that 5c8 Ag is a novel, activation-induced surface T cell protein that is involved in mediating a contact-dependent element of the helper effector function of CD4+ T lymphocytes.
CD4+ T淋巴细胞为B细胞提供接触依赖性刺激,这在一个被称为T辅助功能的过程中对特异性抗体反应的产生至关重要。介导这种功能的活化CD4+ T细胞表面结构尚不完全清楚。我们之前报道了从Jurkat白血病T细胞系中分离出一个功能独特的亚克隆(D1.1),其组成性表达接触依赖性辅助效应功能。为了鉴定介导接触依赖性T辅助功能的T细胞表面分子,产生了一种名为5c8的单克隆抗体(mAb),它可抑制D1.1介导的B细胞活化,并从表面碘化的D1.1细胞中免疫沉淀出一种新的30-kD蛋白质结构。正常CD4+ T细胞在被佛波酯肉豆蔻酸酯和植物血凝素激活后5-6小时短暂表达5c8抗原(Ag),活化后5-6小时表达量最高,24小时后不表达。相比之下,静止或活化的CD8+ T细胞均不表达5c8 Ag。在功能研究中,mAb 5c8抑制固定的活化CD4+ T细胞诱导B细胞表面CD23表达的能力。此外,mAb 5c8抑制CD4+ T细胞指导由商陆有丝分裂原驱动的B细胞终末分化的能力。综上所述,这些数据表明5c8 Ag是一种新的、活化诱导的表面T细胞蛋白,参与介导CD4+ T淋巴细胞辅助效应功能的接触依赖性成分。