Genetic control of immune responses in vitro. V. Stimulation of suppressor T cells in nonresponder mice by the terpolymer L-glutamic acid 60-L-alanine 30-L-tyrosine 10 (GAT).
Genetic control of immune responses in vitro. V. Stimulation of suppressor T cells in nonresponder mice by the terpolymer L-glutamic acid 60-L-alanine 30-L-tyrosine 10 (GAT).
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DOI：
10.1084/jem.140.3.648
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发表时间：
1974-09-01
影响因子：
15.3
通讯作者：
Benacerraf, B
中科院分区：
文献类型：
--
作者：
Kapp, J A;Pierce, C W;Schlossman, S;Benacerraf, B
在最近的研究中，我们发现GAT不仅不能在无应答小鼠中引起GAT特异性应答，而且还会特异性地降低无应答小鼠对GAT结合免疫原性载体MBSA的后续攻击产生GAT特异性PFC应答的能力。本文的研究表明，体内对GAT无反应的DBA/1小鼠的B细胞在体外对GAT- mbsa有反应，如果在培养物中加入外源的载体T细胞。无应答性被证明是gat启动小鼠脾细胞中载体特异性辅助性t细胞功能受损的结果。gat诱导小鼠脾脏细胞特异性抑制GAT-MBSA培养的正常DBA/1小鼠脾脏细胞的gat特异性PFC反应。用抗θ血清加C或X照射预处理gat诱导的脾细胞可防止这种抑制。抑制细胞仅限于含有θ-阳性细胞和少数不含igg细胞的柱纯化淋巴细胞的部分，证实了抑制细胞是T细胞。讨论了这些数据对我们理解免疫反应的铁基因调控的意义。
In recent studies we have found that GAT not only fails to elicit a GAT-specific response in nonresponder mice but also specifically decreases the ability of nonresponder mice to develop a GAT-specific PFC response to a subsequent challenge with GAT bound to the immunogenic carrier, MBSA. Studies presented in this paper demonstrate that B cells from nonresponder, DBA/1 mice rendered unresponsive by GAT in vivo can respond in vitro to GAT-MBSA if exogenous, carrier-primed T cells are added to the cultures. The unresponsiveness was shown to be the result of impaired carrier-specific helper T-cell function in the spleen cells of GAT-primed mice. Spleen cells from GAT-primed mice specifically suppressed the GAT-specific PFC response of spleen cells from normal DBA/1 mice incubated with GAT-MBSA. This suppression was prevented by pretreatment of GAT-primed spleen cells with anti-θ serum plus C or X irradiation. Identification of the suppressor cells as T cells was confirmed by the demonstration that suppressor cells were confined to the fraction of the column-purified lymphocytes which contained θ-positive cells and a few non-Ig-bearing cells. The significance of these data to our understanding of Ir-gene regulation of the immune response is discussed.