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Interestingly, only a portion of the infected mice become patent, which reflects the situation in human individuals infected with <jats:italic>Wuchereria bancrofti<\/jats:italic>. Since those individuals had differing filarial\u2010specific profiles, this study compared differences in immune responses between Mf<jats:sup>+<\/jats:sup> and Mf<jats:sup>\u2013<\/jats:sup> infected <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice. We demonstrate that cultures of total spleen or mediastinal lymph node cells from Mf<jats:sup>+<\/jats:sup> mice produce significantly more interleukin\u20105 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20105) to filarial antigens but equal levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 when compared with Mf<jats:sup>\u2013<\/jats:sup> mice. However, isolated <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells from Mf<jats:sup>+<\/jats:sup> mice produced significantly higher amounts of all measured cytokines, including <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, when compared with <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell responses from Mf<jats:sup>\u2013<\/jats:sup> mice. Since adaptive immune responses are influenced by triggering the innate immune system we further studied the immune profiles and parasitology in infected Toll\u2010like receptor\u20102\u2010deficient (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2<jats:sup>\u2212\/\u2212<\/jats:sup>) and <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4<jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice. Ninety\u2010three per\u00a0cent of <jats:italic>L.\u00a0sigmodontis<\/jats:italic>\u2010exposed <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4<jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice became patent (Mf<jats:sup>+<\/jats:sup>) although worm numbers remained comparable to those in Mf<jats:sup>+<\/jats:sup> wild\u2010type controls. Lack of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 had no influence on patency outcome or worm burden but infected Mf<jats:sup>+<\/jats:sup> mice had significantly lower numbers of Foxp3<jats:sup>+<\/jats:sup> regulatory T cells and dampened peripheral immune responses. Interestingly, <jats:italic>in\u00a0vitro<\/jats:italic> culturing of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells from infected wild\u2010type mice with granulocyte\u2013macrophage colony\u2010stimulating factor\u2010derived <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2<jats:sup>\u2212\/\u2212<\/jats:sup> dendritic cells resulted in an overall diminished cytokine profile to filarial antigens. Hence, triggering <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 or <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 during chronic filarial infection has a significant impact on patency and efficient <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell responses, respectively.<\/jats:p>","DOI":"10.1111\/imm.12573","type":"journal-article","created":{"date-parts":[[2015,12,30]],"date-time":"2015-12-30T11:48:37Z","timestamp":1451476117000},"page":"429-442","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Patency of <i>Litomosoides sigmodontis<\/i> infection depends on <scp>T<\/scp>oll\u2010like receptor 4 whereas <scp>T<\/scp>oll\u2010like receptor 2 signalling influences filarial\u2010specific <scp>CD<\/scp>4<sup>+<\/sup> T\u2010cell responses"],"prefix":"10.1111","volume":"147","author":[{"given":"Maria B.","family":"Rodrigo","sequence":"first","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandy","family":"Schulz","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanessa","family":"Krupp","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Ritter","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katharina","family":"Wiszniewsky","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathrin","family":"Arndts","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, Immunology and Parasitology (IMMIP) University Hospital of Bonn Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth S. 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