{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T08:09:20Z","timestamp":1793261360534,"version":"4.5.0"},"reference-count":89,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"815","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2025,9,10]]},"abstract":"<jats:p>\n                    IFN-\u03b2, a type I interferon, has been used as a first-line therapy for patients with multiple sclerosis (MS) for more than 30 years; however, the cellular and molecular basis of its therapeutic efficacy remains unclear. Here, we first used experimental autoimmune encephalomyelitis (EAE), a mouse model for MS, to show that the therapeutic effects of IFN-\u03b2 were associated with a down-regulation of microRNA-21 (miR-21) and pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 (pT\n                    <jats:sub>H<\/jats:sub>\n                    17) cells. In vitro experiments demonstrated that genetic knockout of miR-21 directly inhibited pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 cell differentiation. Further mechanistic investigations revealed that miR-21 promoted pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 differentiation by inhibiting the transcription factor\n                    <jats:italic toggle=\"yes\">Forkhead box protein O1<\/jats:italic>\n                    (\n                    <jats:italic toggle=\"yes\">Foxo1<\/jats:italic>\n                    ). Accordingly, miR-21 loss abrogated pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 differentiation and conferred resistance to EAE. Treatment of T cell monocultures with IFN-\u03b2 showed that IFN-\u03b2 did not directly limit miR-21 expression. Instead, IFN-\u03b2 treatment inhibited the secretion of miR-21\u2013inducing cytokines from myeloid cells, reduced miR-21 induction within cocultured T cells, and inhibited pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 development. In patient samples, immunophenotypic and targeted transcriptomic analyses revealed that compared with IFN-\u03b2 treatment responders, nonresponders expressed elevated miR-21\u2013inducing cytokines within myeloid cells, alongside increased miR-21 and pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 cytokines within CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Direct miR-21 inhibition reduced pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 differentiation in nonresponder CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells. These results suggest that type I IFN signaling limits central nervous system autoimmunity by inhibiting miR-21\u2013mediated pathogenic T\n                    <jats:sub>H<\/jats:sub>\n                    17 development. miR-21 inhibition may be of potential therapeutic value specifically for the IFN-\u03b2 nonresponder cohort.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adp5802","type":"journal-article","created":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T17:58:14Z","timestamp":1757527094000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":5,"title":["Type I interferon limits central nervous system autoimmunity by modulating the microRNA-21\u2013FOXO1 axis in pathogenic T helper 17 cells"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9152-2880","authenticated-orcid":true,"given":"Johnna Francis","family":"Varghese","sequence":"first","affiliation":[{"name":"Ann 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