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The host transcription factor BHLHE40 is essential for controlling M. tuberculosis infection, in part by repressing Il10 expression, where excess IL-10 contributes to the early susceptibility of Bhlhe40\u2212\/\u2212 mice to M. tuberculosis infection. Deletion of Bhlhe40 in lung macrophages and dendritic cells is sufficient to increase the susceptibility of mice to M. tuberculosis infection, but how BHLHE40 impacts macrophage and dendritic cell responses to M. tuberculosis is unknown. In this study, we report that BHLHE40 is required in myeloid cells exposed to GM-CSF, an abundant cytokine in the lung, to promote the expression of genes associated with a proinflammatory state and better control of M. tuberculosis infection. Loss of Bhlhe40 expression in murine bone marrow\u2013derived myeloid cells cultured in the presence of GM-CSF results in lower levels of proinflammatory associated signaling molecules IL-1\u03b2, IL-6, IL-12, TNF-\u03b1, inducible NO synthase, IL-2, KC, and RANTES, as well as higher levels of the anti-inflammatory\u2013associated molecules MCP-1 and IL-10 following exposure to heat-killed M. tuberculosis. Deletion of Il10 in Bhlhe40\u2212\/\u2212 myeloid cells restored some, but not all, proinflammatory signals, demonstrating that BHLHE40 promotes proinflammatory responses via both IL-10\u2013dependent and \u2013independent mechanisms. In addition, we show that macrophages and neutrophils within the lungs of M. tuberculosis\u2013infected Bhlhe40\u2212\/\u2212 mice exhibit defects in inducible NO synthase production compared with infected wild-type mice, supporting that BHLHE40 promotes proinflammatory responses in innate immune cells, which may contribute to the essential role for BHLHE40 during M. tuberculosis infection in vivo.<\/jats:p>","DOI":"10.4049\/jimmunol.2200819","type":"journal-article","created":{"date-parts":[[2024,4,29]],"date-time":"2024-04-29T09:55:30Z","timestamp":1714384530000},"page":"1766-1781","source":"Crossref","is-referenced-by-count":7,"title":["BHLHE40 Regulates Myeloid Cell Polarization through IL-10\u2013Dependent and \u2013Independent Mechanisms"],"prefix":"10.1093","volume":"212","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0644-6519","authenticated-orcid":false,"given":"Skyler V","family":"Hendrix","sequence":"first","affiliation":[{"name":"Department of Molecular Microbiology, 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Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4767-1680","authenticated-orcid":false,"given":"Asya","family":"Smirnov","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, Center for Women\u2019s Infectious Disease Research, Washington, University School of Medicine , St. Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5887-8826","authenticated-orcid":false,"given":"Sthefany M","family":"Chavez","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, Center for Women\u2019s Infectious Disease Research, Washington, University School of Medicine , St. Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Hie","sequence":"additional","affiliation":[{"name":"Ragon Institute of MGH, MIT, and Harvard , Cambridge, Massachusetts"},{"name":"Department of Biological 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