T CELL REGULATION OF B CELL ACTIVATION

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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.