T CELL REGULATION OF B CELL ACTIVATION

以前的研究表明，抗原介导的B细胞反应 特异性T辅助细胞由T抑制细胞通过两种途径调节 不同的MHC受限路径。后来证明， Lyt1+2-L3T4+抗原特异性和MHC限制性克隆 抑制细胞也可以在这些T细胞中介导抑制效应功能。 依赖抗体反应。克隆的T抑制细胞的功能 通过抗原抑制克隆的T辅助细胞介导的应答 特定的机制需要三方，抗原桥联的相互作用 T抑制细胞、T辅助细胞和反应性B细胞。 针对同基因I-A或I-E产物的自身反应性T细胞克隆 T辅助细胞通过两条不同的途径发挥作用：一条 途径是多克隆的，MHC在T辅助B细胞水平上不受限制 另一种是MHC受到限制并依赖于抗原 反应B细胞的特定触发。已经证明，MHC 限制的、非抗原特异性的抑制子群体，其功能是 通过携带者特异性T辅助细胞调节反应也起到 调节自身反应性T辅助细胞介导的反应。激活 B细胞的抗原特异性和自身反应性T辅助细胞因此 似乎也容易受到类似监管影响的影响。 T细胞在调节B细胞抗体特异性中的作用 通过检测T15独特型对 磷胆碱(PC)。研究发现，克隆的载体种群 特异性和MHC限制性T辅助细胞能够支持T15 合适单倍型的非激发B细胞的独特型显性反应。 这些调查结果表明，对 独特型特异型TH2细胞参与优化子的产生 本实验系统中的独特型显性反应。

It was previously demonstrated that B cell responses mediated by antigen specific T helper cells were regulated by T suppressor cells through two distinct MHC restricted pathways. It was subsequently demonstrated that cloned lines of Lyt1+ 2-L3T4+ antigen specific and MHC restricted suppressor cells could also mediate suppressor effector function in these T dependent antibody responses. Cloned T suppressor cells functioned to suppress the responses mediated by cloned T helper cells through an antigen specific mechanism requiring the tripartite, antigen-bridged interaction of T suppressor cells, T helper cells, and responding B cells. Autoreactive T cell clones, specific for syngeneic I-A or I-E products were shown to function as T helper cells through two distinct pathways: One pathway was polyclonal and MHC unrestricted at the level of T helper-B cell interaction and the other was MHC restricted and dependent upon antigen specific triggering of responding B cells. It has been shown that MHC restricted, antigen-nonspecific suppressor populations which function to regulate responses by carrier specific T helper cells also function to regulate the responses mediated by autoreactive T helper cells. Activation of B cells by antigen specific and autoreactive T helper cells therefore appears to share susceptibility to similar regulatory influences. The role of T cells in regulating the fine specificity of B cell antibody responses was studied by examining the T15 idiotype dominant response to phosphocholine (PC). It was found that cloned populations of carrier specific and MHC restricted T helper cells were capable of supporting T15 idiotype dominant responses in unprimed B cells of appropriate haplotype. These findings demonstrated that no absolute requirement exists for the participation of idiotype specific TH2 cells in the generation of optimally idiotype dominant responses in this experimental system.