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However, the underlying mechanisms to the beneficial effects of IFN-\u03b3 are not well understood. In this study, we found that IFN-\u03b3 exerts therapeutic effects on chronic, relapsing-remitting, and chronic progressive EAE models. The frequency of regulatory T (Treg) cells in spinal cords from chronic EAE mice treated with IFN-\u03b3 was significantly increased with no effect on Th1 and Th17 cells. Consistently, depletion of FOXP3-expressing cells blocked the protective effects of IFN-\u03b3, indicating that the therapeutic effect of IFN-\u03b3 depends on the presence of Treg cells. However, IFN-\u03b3 did not trigger direct in vitro differentiation of Treg cells. In vivo administration of blocking antibodies against either interleukin (IL)-10, transforming growth factor (TGF)-\u03b2 or program death (PD)-1, revealed that the protective effects of IFN-\u03b3 in EAE were also dependent on TGF-\u03b2 and PD-1, but not on IL-10, suggesting that IFN-\u03b3 might have an indirect role on Treg cells acting through antigen-presenting cells. Indeed, IFN-\u03b3 treatment increased the frequency of a subset of splenic CD11b<jats:sup>+<\/jats:sup> myeloid cells expressing TGF-\u03b2-Latency Associated Peptide (LAP) and program death ligand 1 (PD-L1) in a signal transducer and activator of transcription (STAT)-1-dependent manner. Furthermore, splenic CD11b<jats:sup>+<\/jats:sup> cells from EAE mice preconditioned in vitro with IFN-\u03b3 and myelin oligodendrocyte glycoprotein (MOG) peptide exhibited a tolerogenic phenotype with the capability to induce conversion of na\u00efve CD4<jats:sup>+<\/jats:sup> T cells mediated by secretion of TGF-\u03b2. Remarkably, adoptive transfer of splenic CD11b<jats:sup>+<\/jats:sup> cells from IFN-\u03b3-treated EAE mice into untreated recipient mice ameliorated clinical symptoms of EAE and limited central nervous system infiltration of mononuclear cells and effector helper T cells. These results reveal a novel cellular and molecular mechanism whereby IFN-\u03b3 promotes beneficial effects in EAE by endowing splenic CD11b<jats:sup>+<\/jats:sup> myeloid cells with tolerogenic and therapeutic activities.<\/jats:p>","DOI":"10.1186\/s12974-024-03126-3","type":"journal-article","created":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T15:03:02Z","timestamp":1717167782000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Therapeutic role of interferon-\u03b3 in experimental autoimmune encephalomyelitis is mediated through a tolerogenic subset of splenic CD11b+ myeloid cells"],"prefix":"10.1186","volume":"21","author":[{"given":"Gabriel","family":"Arellano","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Acu\u00f1a","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eileah","family":"Loda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lindsay","family":"Moore","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan E.","family":"Tichauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristian","family":"Castillo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabian","family":"Vergara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paula I.","family":"Burgos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo","family":"Penaloza-MacMaster","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen D.","family":"Miller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodrigo","family":"Naves","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,5,31]]},"reference":[{"key":"3126_CR1","doi-asserted-by":"publisher","first-page":"545","DOI":"10.1038\/nri3871","volume":"15","author":"CA Dendrou","year":"2015","unstructured":"Dendrou CA, Fugger L, Friese MA. 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