Ethanol Impairs Major Histocompatibility Complex (MHC) Class II Molecule-Mediated But not MHC Class I Molecule-Mediated T Cell Response in Alcohol-Consuming Mice

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Abstract
The goal of this study was to determine whether alcohol affects alloantigen-induced proliferative and cytolytic activity of T cells in mice, and whether the altered immune response was in part due to a defect of IL-2 activity. The ability of spleen cells from individual alcohol-consuming C57BL/6 mice to generate allo-specific mixed lymphocyte response (MLR) and cytotoxic T lymphocyte (CTL) was compared to that of mice fed on an isocaloric maltose diet and regular diet. Allospecific MLR and CTL were generated by sensitizing spleen cells of C57BL/6 mice against spleen cells from BALB/c mice, and the allo-specific CTL activity was determined by the ability of the CTL to kill 51Cr-labeled P815 mastocytoma target cells. Our results showed that the allo-specific MLR of the responder cells from alcohol-consuming mice was significantly reduced (40% reduction, p > 0.01), and the addition of exogenous interleukin 2 (IL-2) could not reverse the suppression of MLR induced by ethanol. However, our results clearly showed that ethanol has little suppressive effect on allo-reactive CTL of alcohol-consuming mice as compared to the alloreactivity of the control mice (P < 0.05). Finally, we also demonstrated that ethanol did not impair the alloantigen-induced IL-2 production in the mixed lymphocyte cultures (P < 0.1). This study was supported by VA Medical Funds and a grant from the Alcoholic Beverage Medical Research Foundation. We are grateful to Mr. Jerry Sproul for help preparing this manuscript.