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Mouse models of the disease have identified strains that are resistant (<jats:italic>e.g.<\/jats:italic>DBA\/2) or susceptible (<jats:italic>e.g.<\/jats:italic>C57BL\/6) to these pathogens. However, the genetic and immunological basis for this difference has not been fully characterized.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Microarray technology was used to identify genes that were differentially expressed in lung tissue between resistant DBA\/2 and sensitive C57BL\/6 mice after infection with<jats:italic>C. immitis<\/jats:italic>. Differentially expressed genes were mapped onto biological pathways, gene ontologies, and protein interaction networks, which revealed that innate immune responses mediated by Type II interferon (<jats:italic>i.e.<\/jats:italic>,<jats:italic>IFNG<\/jats:italic>) and the signal transducer and activator of transcription 1 (<jats:italic>STAT1<\/jats:italic>) contribute to the resistant phenotype. In addition, upregulation of hypoxia inducible factor 1A (<jats:italic>HIF1A<\/jats:italic>), possibly as part of a larger inflammatory response mediated by tumor necrosis factor alpha (<jats:italic>TNFA<\/jats:italic>), may also contribute to resistance. Microarray gene expression was confirmed by real-time quantitative PCR for a subset of 12 genes, which revealed that<jats:italic>IFNG HIF1A<\/jats:italic>and<jats:italic>TNFA<\/jats:italic>, among others, were significantly differentially expressed between the two strains at day 14 post-infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results confirm the finding that DBA\/2 mice express more Type II interferon and interferon stimulated genes than genetically susceptible strains and suggest that differential expression of<jats:italic>HIF1A<\/jats:italic>may also play a role in protection.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2180-12-218","type":"journal-article","created":{"date-parts":[[2012,9,24]],"date-time":"2012-09-24T22:11:25Z","timestamp":1348524685000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Factors regulated by interferon gamma and hypoxia-inducible factor 1A contribute to responses that protect mice from Coccidioides immitisinfection"],"prefix":"10.1186","volume":"12","author":[{"given":"Christopher H","family":"Woelk","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jin X","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lorraine","family":"Walls","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suganya","family":"Viriyakosol","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akul","family":"Singhania","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Theo N","family":"Kirkland","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joshua","family":"Fierer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2012,9,24]]},"reference":[{"key":"1793_CR1","doi-asserted-by":"publisher","first-page":"73","DOI":"10.2307\/3761847","volume":"94","author":"MC Fisher","year":"2002","unstructured":"Fisher MC, Koenig GL, White TJ, Taylor JW: Molecular and phenotypic description of Coccidioides posadasii sp. nov., previously recognized as the non-California population of Coccidioides immitis. 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