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In susceptible C57BL\/6 (B6) mice, the murine retroviral isolate LP-BM5 induces splenomegaly, hypergammaglobulinemia, profound B- and T-cell immunodeficiency, and increased susceptibility to opportunistic pathogens and terminal B-cell lymphomas. Here, we report that B6.PD-1 (programmed death-1) and B6.IL-10 knockout mice are substantially more susceptible to LP-BM5-induced disease than wild-type B6 mice. LP-BM5-infected B6.PD-1<jats:sup>\u2212\/\u2212<\/jats:sup>mice developed more severe splenomegaly, hypergammaglobulinemia, and immunodeficiency than infected B6 mice: PD-1<jats:sup>\u2212\/\u2212<\/jats:sup>mice are more susceptible to lower doses of LP-BM5 and show more exaggerated disease early postinfection. LP-BM5-infected B6.IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice also develop exaggerated LP-BM5-induced disease, compared to B6 mice, without a significant change in the retroviral load. By reciprocal reconstitution experiments, comparing wild-type versus PD-1<jats:sup>\u2212\/\u2212<\/jats:sup>sources of the requisite cells for LP-BM5 pathogenesis\u2014CD4 T and B cells, PD-1<jats:sup>+<\/jats:sup>B cells appear to be crucial in the normal limitation of LP-BM5-induced disease in B6 mice. Also, infected B6 mice have increased CD11b<jats:sup>+<\/jats:sup>spleen cells that express interleukin-10 (IL-10). However, PD-1<jats:sup>\u2212\/\u2212<\/jats:sup>mice, though showing an even greater expansion of CD11b<jats:sup>+<\/jats:sup>cells after LP-BM5 inoculation, did not show an equivalent increase in IL-10-producing cells. Thus, it appears that PD-1\/PD-L interactions and IL-10 are primarily important in moderating the effects of LP-BM5-induced disease in B6 mice.<\/jats:p>","DOI":"10.1128\/jvi.01665-07","type":"journal-article","created":{"date-parts":[[2007,12,20]],"date-time":"2007-12-20T01:53:51Z","timestamp":1198115631000},"page":"2456-2469","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["The Programmed Death-1 and Interleukin-10 Pathways Play a Down-Modulatory Role in LP-BM5 Retrovirus-Induced Murine Immunodeficiency Syndrome"],"prefix":"10.1128","volume":"82","author":[{"given":"Kathy A.","family":"Green","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Dartmouth Medical School, and Norris Cotton Cancer Center, Lebanon, New Hampshire 03756"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Taku","family":"Okazaki","sequence":"additional","affiliation":[{"name":"Department of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606-8501, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tasuku","family":"Honjo","sequence":"additional","affiliation":[{"name":"Department of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606-8501, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. 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