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The manner in which minor histocompatibility (H) antigens have been defined in mouse and man, in vivo and in vitro, is considered. Chromosomal mapping of minor H genes using T-cell clones is illustrated, with particular reference to the H-Y antigen gene, using the sex-reversing translocation Sxr of mouse and the Sxr' mutation derived from it. A number of minor H antigen-specific T-cell clones restricted by class I or class II major histocompatibility complex (MHC) molecules are described, together with information about their phenotypes and T-cell receptor usage. [ABSTRACT FROM AUTHOR]

Sex reversed X/X male mice carrying Sxr or the variant Sxr' were typed for expression of the male specific histocompatibility antigen H-Y, by skin grafting and by in vitro cytotoxic and proliferative tests. The X/XSxr males, like X/Y males, were Hey positive by in vitro testing, and failed to reject semiesyngeneic male skin grafts. In contrast X/XSxr' males, like xix females, were H-Y negative and rejected semi-syngeneic, male skin. Spleen cells from X/Y males sensitized C57BL/10 female recipients to reject syngeneic male skin rapidly, whilst immunization with X/X female or X/XSxr' male cells failed to stimulate such second-set responses. These data suggest that the H-Y antigen detected by cytotoxic T cells is the same as that detected by graft rejection responses, that the Sxr' variant is not a tissue-specific regulatory mutation, and that X/XSxr' individuals do not express H-Y antigen but nevertheless develop as phenotypic males. [ABSTRACT FROM AUTHOR]

We previously reported that Yersinia pseudotuberculosis-derived mitogen (YPM) acts as a superantigen to human T cells. In this study, we assessed the superantigenicity and toxicity of YPM using murine experimental models. YPM activated T cells to produce interleukin-2 in a major histocompatibility complex class II molecule-dependent manner. The T-cell blasts induced by YPM expressed T-cell receptor (TCR) beta-chain variable region (Vbeta)7, Vbeta8.1, Vbeta8.2 and Vbeta8.3. The injection of YPM into mice pre-sensitized with D-galactosamine induced lethal shock. This shock was blocked by the injection of monoclonal antibodies (mAbs) to CD4, TCR Vbeta7 plus Vbeta8, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), but not by injection to CD8 or unrelated Vbeta. These results indicate that YPM-induced shock requires the presence of CD4+ T cells bearing TCR Vbeta7 and Vbeta8, and that endogenous TNF-alpha and IFN-gamma mediate the lethal effects.