Hirohata S, Jelinek D F, Lipsky P E
Department of Internal Medicine, University of Texas Health Science Center, Dallas 75235.
J Immunol. 1988 Jun 1;140(11):3736-44.
The capacity of mAb directed at the CD3 molecular complex (64.1) to induce T cell-dependent B cell proliferation and differentiation was examined. Coculture of B cells with mitomycin C-treated T4 cells (T4 mito) stimulated by immobilized 64.1 resulted in marked B cell proliferation and Ig-secreting cells (ISC) generation in the absence of any additional stimulation. The magnitude of the B cell responses induced by immobilized 64.1-stimulated T4 mito was far greater than that induced by other stimuli, such as Staphylococcus aureus plus factors produced by mitogen-activated T cells, PWM, or soluble 64.1. The induction of maximal B cell responsiveness required direct contact between activated T cells and responding B cells. Of note, immobilized 64.1 also induced B cell proliferation and ISC generation in the presence of mitomycin C-treated T8 cells. By contrast, immobilized 64.1 stimulated T4 or T8 cells that had not been treated with mitomycin C induced very modest ISC generation and suppressed B cell responses supported by T4 mito even in the presence of exogenous IL-2 or factors produced by mitogen-activated T cells. The interactions between T and B cells in these cultures not only induced B cell responses, but also enhanced the production of IL-2 by activated T cells. Increased IL-2 production was facilitated when culture conditions afforded the opportunity for contact between B cells and activated T cells. These results indicate that the establishment of interactions between B cells and anti-CD3-stimulated T4 or T8 cells provides all of the signals necessary for proliferation and differentiation of B cells without other stimuli and also augments the production of lymphokines by the activated T cells. The data emphasize the role of Ag-nonspecific interactions between B cells and T cells in promoting polyclonal responses of both cell types.
研究了针对CD3分子复合物（64.1）的单克隆抗体诱导T细胞依赖性B细胞增殖和分化的能力。在没有任何额外刺激的情况下，将B细胞与经丝裂霉素C处理的T4细胞（T4 mito）共培养，并用固定化的64.1刺激，结果导致显著的B细胞增殖和Ig分泌细胞（ISC）生成。固定化的64.1刺激的T4 mito诱导的B细胞反应强度远大于其他刺激诱导的反应，如金黄色葡萄球菌加丝裂原激活的T细胞产生的因子、PWM或可溶性64.1。诱导最大B细胞反应性需要活化的T细胞与反应性B细胞直接接触。值得注意的是，在存在经丝裂霉素C处理的T8细胞的情况下，固定化的64.1也诱导B细胞增殖和ISC生成。相比之下，固定化的64.1刺激未用丝裂霉素C处理的T4或T8细胞，即使在存在外源性IL-2或丝裂原激活的T细胞产生的因子的情况下，也只能诱导非常适度的ISC生成，并抑制由T4 mito支持的B细胞反应。这些培养物中T细胞与B细胞之间的相互作用不仅诱导了B细胞反应，还增强了活化T细胞产生IL-2的能力。当培养条件为B细胞与活化T细胞之间的接触提供机会时，IL-2的产生增加。这些结果表明，B细胞与抗CD3刺激的T4或T8细胞之间相互作用的建立提供了B细胞增殖和分化所需的所有信号，无需其他刺激，并且还增强了活化T细胞产生淋巴因子的能力。数据强调了B细胞与T细胞之间的抗原非特异性相互作用在促进两种细胞类型的多克隆反应中的作用。
