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Humans and rodents both express Dectin-1 and Toll-like receptor 2 (TLR2) on myeloid cells, and those receptors collaborate to maximize the cytokine\/chemokine responses to spherules (the tissue form of the fungi) and to formalin-killed spherules (FKS). We showed that Dectin-1 is necessary for resistance to pulmonary coccidioidomycosis, but the importance of TLR2\n                    <jats:italic>in vivo<\/jats:italic>\n                    is uncertain. Myeloid differentiation factor 88 (MyD88) is the adapter protein for TLR2 and -4, interleukin-1R1 (IL-1R1), and IL-18R1. MyD88\/TRIF\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    and MyD88\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were equally susceptible to\n                    <jats:named-content content-type=\"genus-species\">C. immitis<\/jats:named-content>\n                    infection, in contrast to C57BL\/6 (B6) controls. Of the four surface receptors, only IL-1R1 was required for resistance to\n                    <jats:named-content content-type=\"genus-species\">C. immitis<\/jats:named-content>\n                    , partially explaining the susceptibility of MyD88\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. We also found that FKS stimulated production of IL-1Ra by bone marrow-derived dendritic cells (BMDCs), independent of MyD88 and Dectin-1. There also was a very high concentration of IL-1Ra in the lungs of infected B6 mice, supporting the potential importance of this regulatory IL-1 family protein in the largely ineffective response of B6 mice to coccidioidomycosis. These results suggest that IL-1R1 signaling is important for defense against\n                    <jats:named-content content-type=\"genus-species\">C. immitis<\/jats:named-content>\n                    infection.\n                  <\/jats:p>","DOI":"10.1128\/iai.00028-18","type":"journal-article","created":{"date-parts":[[2018,4,3]],"date-time":"2018-04-03T08:50:54Z","timestamp":1522745454000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":14,"title":["Myeloid Differentiation Factor 88 and Interleukin-1R1 Signaling Contribute to Resistance to Coccidioides immitis"],"prefix":"10.1128","volume":"86","author":[{"given":"Suganya","family":"Viriyakosol","sequence":"first","affiliation":[{"name":"Department of Medicine, UC San Diego School of Medicine, San Diego, California, USA"},{"name":"VA Healthcare, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorraine","family":"Walls","sequence":"additional","affiliation":[{"name":"VA Healthcare, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon","family":"Okamoto","sequence":"additional","affiliation":[{"name":"Department of Medicine, UC San Diego School of Medicine, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eyal","family":"Raz","sequence":"additional","affiliation":[{"name":"Department of Medicine, UC San Diego School of Medicine, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Surgery, James H. 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