T CELL REGULATION OF B CELL ACTIVATION

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It had previously been demonstrated that B cell antibody responses can be activated by helper T cells through two distinct pathways. Individual cloned T cell populations are in fact capable of mediating both MHC-restricted and non-MHC-restricted pathways of B cell activation. Recent studies have demonstrated the ability of such cloned helper populations to function in the MHC restricted activation of B cells through an IL-2 dependent pathway. B cell responses mediated by antigen specific T helper cells are regulated by T suppressor cells through two distinct MHC restricted pathways. It was subsequently demonstrated that cloned lines of Lyt 1+ 2- L3T4+ antigen specific and MHC restricted suppressor cells could also mediate suppressor effector function in these T dependent antibody responses. 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. 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) and the CRIA dominant response to Ars. It was found that cloned populations of carrier specific and MHC restricted T helper cells were capable of supporting T15 of CRIA idiotype dominant response in 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.