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Herein, we investigated whether <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 prevents excessive host tissue damage during infection with the protozoan parasite, <jats:italic><jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>oxoplasma gondii<\/jats:italic>. Surprisingly, our results demonstrate that <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101\u2010deficient mice have increased susceptibility to <jats:italic><jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>. gondii<\/jats:italic>, with increased parasite cyst counts along with reduced type\u20101 cytokine responses (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012 and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3). <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101<jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s showed no cell intrinsic defect in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012 production in vitro. Instead, <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 neutralization via genetic or pharmacological approaches resulted in a striking increase in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 release, which impaired type\u20101\u2010inflammation during infection. Our results indicate that the absence of <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 increases <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 production even in the absence of infection. Although the possibility that such increased <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 protects against autoimmune damage is speculative, our results show that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 suppresses the development of protective <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1 immune response after <jats:italic><jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>. gondii<\/jats:italic> infection.<\/jats:p>","DOI":"10.1002\/eji.201343658","type":"journal-article","created":{"date-parts":[[2013,10,26]],"date-time":"2013-10-26T05:51:10Z","timestamp":1382766670000},"page":"469-479","source":"Crossref","is-referenced-by-count":22,"title":["<scp>PD<\/scp>\u20101 modulates steady\u2010state and infection\u2010induced <scp>IL<\/scp>\u201010 production in vivo"],"prefix":"10.1002","volume":"44","author":[{"given":"Cortez","family":"McBerry","sequence":"first","affiliation":[{"name":"Division of Immunobiology Cincinnati Children's Hospital Medical Center  Cincinnati OH USA"},{"name":"University of Cincinnati College of Medicine  Cincinnati OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Dias","sequence":"additional","affiliation":[{"name":"Division of Immunobiology Cincinnati Children's Hospital Medical Center  Cincinnati OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathaniel","family":"Shryock","sequence":"additional","affiliation":[{"name":"Division of Immunobiology Cincinnati Children's Hospital Medical Center  Cincinnati OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristin","family":"Lampe","sequence":"additional","affiliation":[{"name":"Division of Immunobiology Cincinnati Children's Hospital Medical Center  Cincinnati OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fredy R. 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