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B6PD-1 knockout mice show more pronounced activational and immunodeficiency disease parameters than prototypic susceptible B6 mice after infection with a murine retrovirus complex, LP-BM5



B6PD-1 knockout mice show more pronounced activational and immunodeficiency disease parameters than prototypic susceptible B6 mice after infection with a murine retrovirus complex, LP-BM5



FASEB Journal 18(4-5): Abst 82 12



C57BL/6 mice infected with the LP-BM5 isolate of murine retroviruses develop splenomegaly, lymphadenopathy, hypergammaglobulinemia, an immunodeficiency state, and terminal B cell lymphomas. Because of the similarities to the pathologies seen in HIV/AIDS, this syndrome has been referred to as mouse AIDS, MAIDS. In MAIDS, CD154/CD40 interactions are required, and CD4+ T and B cells are necessary and sufficient in providing CD154 and CD40 expression. CD40 associated TRAF 6 is necessary for full-blow MAIDS which suggests that TRAF 6-dependent, CD40 signaling is required. The requirement for CD154 ligation of CD40 and TRAF-mediated signaling is not explained by the well-known, CD40-activated up-regulation of CD80 and/or CD86 as CD80/CD86 d.k.o. mice are MAIDS susceptible. We examine here, the role of PD-1 (programmed death receptor-1) in MAIDS by use of k.o. mice. This molecule appears to negatively regulate disease in MAIDS for "optimal dose" LP-BM5 infected PD-1 k.o.&39;s develop disease scoring splenomegaly, and hypergammaglobulinemia in many fold excess, and mitogenic T and B cell responses as several fold lower, as compared to uninfected (-) k.o&39;s, and (+) and (-) B6 mice. Disease severity in (+) PD-1 k.o&39;s was lessened proportionally with limiting virual dose but always exceeded that seen for B6 infected with the same viral dose. Infected PD-1 k.o. mice developed a severe loss of splenic CD19+ cells with increased numbers of CD4+ and CD11b+ cells.

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