Benacerraf B, Kapp J A, Pierce C W, Katz D H
J Exp Med. 1974 Jul 1;140(1):185-98. doi: 10.1084/jem.140.1.185.
The conditions for cooperative interactions between nonresponder B10.S B cells and GAT-primed irradiated (C57BL/6 x SJL)F(1) T cells in the response by cultures of mouse spleen cells to GAT were investigated. GAT-specific antibody responses could be elicited by soluble GAT in cultures of GAT-primed irradiated (C57BL/6 x SJL)F(1) T cells with C57BL/6 B cells but not with B10.S B cells. In contrast, when GAT was presented to the cultures on F(1) macrophages or as aggregates of GAT with MBSA, GAT-specific PFC responses were observed with both B10.S or C57BL/6 B cells. Irradiated GAT-primed T cells were nevertheless essential for the development of these responses. The GAT-specific response of B10.S B cells in these cultures was inhibited by the addition of soluble GAT at culture initiation. These results indicate that genetic disparity at Ir loci is not an absolute barrier to T-B-cell cooperative interactions in the response to antigens under Ir gene control. The significance of these data for the function of Ir gene products in immunocompetent cells is discussed.
研究了在小鼠脾细胞培养物对谷氨酸-丙氨酸-酪氨酸(GAT)的应答中,无反应性B10.S B细胞与经GAT致敏的辐照(C57BL/6×SJL)F1 T细胞之间合作相互作用的条件。在经GAT致敏的辐照(C57BL/6×SJL)F1 T细胞与C57BL/6 B细胞的培养物中,可溶性GAT可引发GAT特异性抗体应答,但与B10.S B细胞则不能。相反,当GAT以F1巨噬细胞呈递给培养物或作为GAT与甲基化牛血清白蛋白(MBSA)的聚集体时,B10.S或C57BL/6 B细胞均观察到GAT特异性的空斑形成细胞(PFC)应答。不过,经辐照的GAT致敏T细胞对于这些应答的发生是必不可少的。在培养开始时添加可溶性GAT可抑制这些培养物中B10.S B细胞的GAT特异性应答。这些结果表明,Ir基因座上的遗传差异并非是Ir基因控制下对抗原应答中T-B细胞合作相互作用的绝对障碍。讨论了这些数据对于免疫活性细胞中Ir基因产物功能的意义。