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Effect of interferon-gamma on the abnormality of T cell activation in NZB mice
M Minoda1, M Funauchi, A Horiuchi
1Third Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.
It is known that New Zealand black (NZB) mice have a defect in the autoantigen recognition mechanism by T cells. The present study was carried out to examine whether the defect could be improved by normalizing the self Ia molecule expression on thymic reticuloepithelial cells (TRC) by using interferon-gamma (IFN-gamma). Syngeneic mixed lymphocyte reaction (SMLR) was used as an indicator of the mechanism of autoantigen recognition. In the reaction, T cells separated from the thymus were used as responders, and machrophages separated from the spleen were used as stimulators. When the responders were cultured with TRC, in which self Ia molecule expressions had been enhanced by IFN-gamma, for activation, the low level of SMLR in NZB mice was elevated close to the normal level. It was suggested, therefore, that IFN-gamma could normalize the defective autoantigen expression on TRC in NZB mice and improve the abnormal T cell activation against autoantigens.
It is known that New Zealand black (NZB) mice have a defect in the autoantigen recognition mechanism by T cells. The present study was carried out to examine whether the defect could be improved by normalizing the self Ia molecule expression on thymic reticuloepithelial cells (TRC) by using interferon-gamma (IFN-gamma). Syngeneic mixed lymphocyte reaction (SMLR) was used as an indicator of the mechanism of autoantigen recognition. In the reaction, T cells separated from the thymus were used as responders, and machrophages separated from the spleen were used as stimulators. When the responders were cultured with TRC, in which self Ia molecule expressions had been enhanced by IFN-gamma, for activation, the low level of SMLR in NZB mice was elevated close to the normal level. It was suggested, therefore, that IFN-gamma could normalize the defective autoantigen expression on TRC in NZB mice and improve the abnormal T cell activation against autoantigens.