Synergy between stimulator cells in the induction of the anti-Mlsa response.
Synergy between stimulator cells in the induction of the anti-Mlsa response.
复制标题
刺激细胞之间在诱导抗 Mlsa 反应中的协同作用。
DOI：
10.1111/j.1744-313x.1988.tb00415.x
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Dorf,ME
中科院分区：
文献类型：
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作者：
DeKruyff,RH;Laning,J;Dorf,ME
我们已经确定了两种类型的克隆响应Mls决定簇。一种类型对来自携带Mlsa刺激决定簇的小鼠的纯化B细胞反应强烈。另一种类型，包括克隆Lyl-N5，对未分级的脾细胞反应强烈，但对单独的B细胞或来自Mlsa荷瘤小鼠的单独的脾粘附细胞（SAC）没有反应。需要两种刺激细胞类型（B细胞和SAC）之间的协同作用来诱导克隆Lyl-N5的Mls应答。克隆Lyl-N5对携带Mlsa的B细胞应答的失败通过添加从携带Mlsballele或非刺激性Mlsballele的小鼠中获得的SAC来逆转。需要B细胞来提供Mls决定子。克隆Ly 1-N5的Mls反应受到H-2 B、H-2 d和H-2 k单倍型共有的II类决定子的限制，但不受H-2 q单倍型的限制。通过使用同时携带Mlsa和允许的H-2同种异体抗原的B细胞获得克隆的最佳应答。然而，在携带Mlsa的B细胞和携带非刺激性Mlsb但携带允许性la表位的非允许性Iaq和SAC之间也观察到互补，导致克隆的激活。SAC提供了某些克隆（如克隆Ly 1-N5）增殖所需的不确定信号，而正常B细胞不提供这种信号。在这份报告中，我们表明，AKTB-lb B-细胞肿瘤系刺激克隆Ly 1-N5的增殖，在SAC的情况下，这表明肿瘤系已经获得了提供这种信号的能力。
We have identified two types of clones responsive to Mls determinants. One type responded vigorously to purified B cells from mice bearing Mlsa‐stimulatory determinants. The other type, including clone Lyl‐N5, responded vigorously to unfractionated spleen cells, but failed to respond to B cells alone or to spleenadherent cells (SAC) alone from the Mlsa‐bearing mice. Synergy between two stimulator cell types, B cells and SAC, was required to induce the Mls response of clone Lyl‐N5. The failure of clone Lyl‐N5 to respond to Mlsa‐bearing B cells was reversed by the addition of SAC taken from mice bearing theMlsballele or the non‐stimulatoryMlsballele. B cells were required to provide the Mlsadeterminant.The Mls response of clone Ly1‐N5 is restricted by class II determinants shared by theH‐2b,H‐2dandH‐2khaplotypes, but not theH‐2qhaplotype. The optimal response of the clone was obtained by using B cells bearing both Mlsaand the permissiveH‐2alloantigen. However, complementation was also observed between B cells bearing Mlsaand the non‐permissive Iaqand SAC bearing the non‐stimulatory Mlsb, but a permissive la epitope, resulting in activation of the clone.Clone Ly1‐N5 responds to Mlsa‐bearing B cells only in the presence of SAC. The SAC provide an undefined signal required for the proliferation of certain clones such as clone Ly1‐N5, which is not provided by normal B cells. In this report, we show that the AKTB‐lb B‐cell tumour line stimulates the proliferation of clone Ly1‐N5, in the absence of SAC, suggesting that the tumour line has acquired the capacity to provide this signal.