{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T16:09:17Z","timestamp":1785427757515,"version":"3.56.0"},"posted":{"date-parts":[[2026,1,28]]},"group-title":"Immunology","reference-count":52,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/"}],"funder":[{"award":["R01AI116885"],"award-info":[{"award-number":["R01AI116885"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R21AI164722"],"award-info":[{"award-number":["R21AI164722"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R01CA241816"],"award-info":[{"award-number":["R01CA241816"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,1,28]]},"abstract":"<jats:title>SUMMARY<\/jats:title>\n                <jats:p>\n                  T\n                  <jats:sub>H<\/jats:sub>\n                  17 cells play a central role in several human autoimmune diseases. We and others reported the nuclear receptor, REV-ERB\u03b1, as a cell-intrinsic repressor of T\n                  <jats:sub>H<\/jats:sub>\n                  17-mediated pathogenicity. REV-ERB\u03b2, REV-ERB\u03b1\u2019s closely related family member, is thought to be functionally redundant to REV-ERB\u03b1, which we sought to explore in T\n                  <jats:sub>H<\/jats:sub>\n                  17-mediated immunity. Our data indicate that deletion of REV-ERB\u03b2 enhances T\n                  <jats:sub>H<\/jats:sub>\n                  17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis. RNA-sequencing indicates REV-ERB\u03b2 and REV-ERB\u03b1 do not have similar transcriptional profiles. REV-ERB\u03b2 does not appear to regulate gene expression through interaction with the classic co-repressor NCoR1, which is in contrast to REV-ERB\u03b1 in T\n                  <jats:sub>H<\/jats:sub>\n                  17 cells, nor does it utilize heme, its known endogenous ligand for its repressive functions. Our results establish that while REV-ERB\u03b2 also acts as a negative regulator of T\n                  <jats:sub>H<\/jats:sub>\n                  17-cell function and pathogenicity, it does so in a manner that is non-redundant, independent, and unique to REV-ERB\u03b1.\n                <\/jats:p>","DOI":"10.64898\/2026.01.26.701826","type":"posted-content","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T05:05:24Z","timestamp":1769663124000},"source":"Crossref","is-referenced-by-count":0,"title":["Negative regulation of T\n                  <sub>H<\/sub>\n                  17-mediated inflammation by the nuclear receptor REV-ERB\u03b2"],"prefix":"10.64898","author":[{"given":"Sean","family":"Campbell","sequence":"first","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah A.","family":"Mosure","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"},{"name":"Skaggs Graduate School of Chemical and Biological Sciences, Scripps Research, La Jolla, CA, USA"},{"name":"Department of Integrative Structural and Computational Biology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammed","family":"Amir","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Chuck","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"},{"name":"Skaggs Graduate School of Chemical and Biological Sciences, Scripps Research, La Jolla, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qun","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8807-0342","authenticated-orcid":false,"given":"Laura A.","family":"Solt","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA"},{"name":"Skaggs Graduate School of Chemical and Biological Sciences, Scripps Research, La Jolla, CA, USA"},{"name":"Department of Molecular Medicine, The Herbert Wertheim UF Scripps Institute for 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