A SIGNIFICANT PROPORTION OF NORMAL RESTING B-CELLS ARE INDUCED TO SECRETE IMMUNOGLOBULIN THROUGH CONTACT WITH ANTI-RECEPTOR ANTIBODY-ACTIVATED HELPER T-CELLS IN CLONAL CULTURES
A SIGNIFICANT PROPORTION OF NORMAL RESTING B-CELLS ARE INDUCED TO SECRETE IMMUNOGLOBULIN THROUGH CONTACT WITH ANTI-RECEPTOR ANTIBODY-ACTIVATED HELPER T-CELLS IN CLONAL CULTURES
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DOI：
10.1002/eji.1830180313
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发表时间：
1988-03-01
影响因子：
5.4
通讯作者：
NOSSAL, GJV
中科院分区：
文献类型：
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作者：
RIEDEL, C;OWENS, T;NOSSAL, GJV
本报告描述了单细胞技术，以解决细胞相互作用的性质，其中活化的T淋巴细胞刺激小的静息B细胞发展成抗体形成细胞克隆的情况下，任何表面免疫球蛋白配体或抗原桥。克隆的T辅助细胞系E9.D4用结合到Teraski 10 μ l培养威尔斯孔塑料上的抗V β 8抗体F23.1刺激。当使用过量的T辅助淋巴细胞时（1000个X射线照射的或600个未照射的、刺激的E9. D4细胞），10-25%的B细胞通过抗体形成应答，这通过培养5天后进行的酶联免疫吸附测定来判断。当存在一个或非常少量的B细胞时，抗体形成细胞形成的限速步骤是存在的T细胞的数量。当倾斜培养盘以迫使T和B细胞靠近在培养威尔斯底部边缘形成的沟时，很少的T细胞足以刺激。当T细胞数量有限时，未照射的T细胞的表现优于照射的T细胞。一些保持7天的细胞克隆转向生产IgG抗体。E9.D4上清液在引起B细胞刺激方面几乎无效，即使当加入3 T3填充细胞以支持培养物时也是如此。结果表明，细胞与强活化T细胞的接触，以及可能的结合物形成，可以引起邻近静息B细胞的变化，类似于IG受体交联的变化，随后淋巴因子通量（即使不涉及IL 4和IL 5）促进抗体形成细胞的发育。
This report describes single-cell techniques to address the nature of a cellular interaction in which activated T lymphocytes stimulate small resting B cells to develop into antibody-forming cell clones in the absence of any surface immunoglobulin ligand or an antigen bridge. The cloned T helper cell line E9.D4 was stimulated with the anti-V.beta.8 antibody F23.1 bound to the plastic of Teraski 10-.mu.l culture wells. When an excess of T helper lymphocytes was used (1000 X-irridated or 600 unirradiated, stimulated E9.D4 cells), 10-25% of B cells responded by antibody formation as judged by an enzyme-linked immunosorbent assay performed after 5 days of culture. When one or a very small number of B cells were present, the rate-limiting step to antibody-forming cell formation was the number of T cells present. Far fewer T cells sufficed for stimulation when culture trays were tilted to force T and B cells into proximity at the sulcus formed at the botton edge of culture wells. When T cell numbers were limiting, unirradiated T cells out-performed irradiated T cells. Some cell clones held for 7 days switched to IgG antibody production. E9.D4 supernatants were virtually ineffective in causing B cell stimulation, even when 3T3 filler cells were added to support cultures. The result suggest that cell contact, and perhaps conjugate formation, with a strongly activated T cell can cause changes in the adjacent resting B cells akin to those of Ig receptor cross-linking, following which a lymphokine flux (even one not involving IL 4 and 5) promotes antibody-forming cell development.