LACK OF MMTV SUPERANTIGEN PRESENTATION IN MHC CLASS II-DEFICIENT MICE

Mammary tumor viruses (MMTVs) as well as their endogenous counterparts encode superantigens which react with T cells expressing particular T cell receptor Vp chains, Several lines of evidence indicated that MHC class II is required for the functional presentation of these superan tigens, Here we provide direct proof that the function of superantigen s is abrogated in the absence of MHC class II expression. No deletion of MIs-1-reactive T cells was observed in MHC class II-deficient mice, and splenocytes from these animals did not stimulate MIs-1-reactive T cell hybrids in vitro. Furthermore, the viral spread in MHC class II- deficient mice, maternally infected with MMTV(C3H), was severely reduc ed. While initial infection in the gut-associated lymphocytes was comp arable between MHC class II-deficient and normal mice, the level of in fection in the spleen and the mammary tissue was much lower in the def icient animals. Quantitation of proviral DNA in spleen revealed a dire ct correlation between the magnitude of superantigen stimulation and d egree of infection. These experiments document the direct effect of su perantigen stimulation on viral amplification. (C) 1996 Academic Press , Inc.