Yellin M J, Lee J J, Chess L, Lederman S
Department of Medicine, Columbia University, New York, NY 10032.
J Immunol. 1991 Nov 15;147(10):3389-95.
Helper T lymphocytes provide a contact dependent signal to resting B cells that is required for optimal differentiation into Ig-secreting cells. The surface structure(s) on T cells that mediate helper function have not been identified but are known to be induced by T cell activation. A CD4- subclone of the Jurkat leukemic T cell line (D1.1) was isolated and found to be distinct from CD4+ Jurkat clones and a variety of other T and non-T cell leukemic lines in that coculture of D1.1 with resting B cells induced B cells to specifically express surface CD23 molecules, a marker of B cell activation. Furthermore, Jurkat D1.1 induced B cell proliferation and terminal B cell differentiation into IgG-secreting cells in the presence of T cell-dependent B cell mitogens. Similar to the helper effector function of activated T cells, the effects of Jurkat D1.1 were neither Ag nor MHC restricted. Paraformaldehyde fixed Jurkat D1.1 cells remained competent to activate B cells while D1.1 supernatants and diffusible factors were inactive. The effect of Jurkat D1.1 on B cell activation was distinct from that of rIL-4 and was not inhibited by antibodies to IL-4. Together these observations suggested that surface structures on D1.1 and not secreted factors, mediated contact-dependent helper effector function.
辅助性T淋巴细胞向静止的B细胞提供一种接触依赖性信号，这是B细胞最佳分化为分泌免疫球蛋白细胞所必需的。介导辅助功能的T细胞表面结构尚未明确，但已知是由T细胞活化诱导产生的。分离出Jurkat白血病T细胞系（D1.1）的一个CD4-亚克隆，发现它与CD4+ Jurkat克隆以及多种其他T和非T细胞白血病系不同，因为D1.1与静止B细胞共培养可诱导B细胞特异性表达表面CD23分子，这是B细胞活化的一个标志物。此外，在存在T细胞依赖性B细胞有丝分裂原的情况下，Jurkat D1.1可诱导B细胞增殖并使其终末分化为分泌IgG的细胞。与活化T细胞的辅助效应功能相似，Jurkat D1.1的作用既不受抗原限制也不受主要组织相容性复合体（MHC）限制。多聚甲醛固定的Jurkat D1.1细胞仍有激活B细胞的能力，而D1.1的上清液和可扩散因子则无活性。Jurkat D1.1对B细胞活化的作用与重组白细胞介素-4（rIL-4）不同，且不受抗IL-4抗体的抑制。这些观察结果共同表明，介导接触依赖性辅助效应功能的是D1.1的表面结构而非分泌因子。
