{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T02:12:44Z","timestamp":1789524764464,"version":"build-2803163510"},"reference-count":132,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"113","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2025,11,7]]},"abstract":"<jats:p>\n                    T helper 17 (T\n                    <jats:sub>H<\/jats:sub>\n                    17) cells are found in the periphery and synovium of patients with rheumatoid arthritis (RA); however, IL-17\u2013targeted interventions have limited efficacy in established RA. Inflammation can induce T\n                    <jats:sub>H<\/jats:sub>\n                    17 cell transdifferentiation into IL-17\u2013negative exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cells, but the role of exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cells in arthritis is unknown. We performed T\n                    <jats:sub>H<\/jats:sub>\n                    17 cell lineage tracing in the SKG mouse model of RA. In arthritic mice, synovial T\n                    <jats:sub>H<\/jats:sub>\n                    17 cells transdifferentiate into CD44\n                    <jats:sup>+<\/jats:sup>\n                    exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cells, which are more arthritogenic and sustain inflammation that is IL-17 independent. The exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cell gene signature includes up-regulation of CD44 and sphingosine-1-phosphate receptor 4 (S1PR4) and correlates with the profile of human RA synovial CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells. We demonstrate that cross-talk between T\n                    <jats:sub>H<\/jats:sub>\n                    17 cells and fibroblast-like synoviocytes (FLSs) via S1P promotes T\n                    <jats:sub>H<\/jats:sub>\n                    17-exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cell conversion. CD44 is necessary for exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cell\u2013mediated arthritis. Our study suggests that FLS expansion during RA progression promotes T\n                    <jats:sub>H<\/jats:sub>\n                    17-exT\n                    <jats:sub>H<\/jats:sub>\n                    17 cell conversion. These results could potentially enable RA precision therapy.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.adm7800","type":"journal-article","created":{"date-parts":[[2025,11,7]],"date-time":"2025-11-07T18:58:12Z","timestamp":1762541892000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":9,"title":["T\n                    <sub>H<\/sub>\n                    17 cells converted into exT\n                    <sub>H<\/sub>\n                    17 cells sustain rheumatoid-like IL-17\u2013independent inflammatory arthritis"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1631-0866","authenticated-orcid":true,"given":"Martina","family":"Zoccheddu","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, Allergy and Immunology, University of California, San Diego, La Jolla, CA 92093, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3107-788X","authenticated-orcid":true,"given":"Kensuke","family":"Suga","sequence":"additional","affiliation":[{"name":"Department of Medicine, Kao Autoimmunity Institute and Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7077-5969","authenticated-orcid":true,"given":"Amara","family":"Seng","sequence":"additional","affiliation":[{"name":"Department of Medicine, Kao Autoimmunity Institute and Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8077-9824","authenticated-orcid":true,"given":"Mattias N. D.","family":"Svensson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, Allergy and Immunology, University of California, San Diego, La Jolla, CA 92093, USA."},{"name":"Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, Institute of Medicine, University of Gothenburg, Gothenburg 41346, Sweden."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paramita","family":"Dutta","sequence":"additional","affiliation":[{"name":"Centers for Autoimmunity, Inflammation and Cancer Immunotherapy, La Jolla Institute for Immunology, La Jolla, CA 92037, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9253-4891","authenticated-orcid":true,"given":"Sanaz","family":"Panahandeh","sequence":"additional","affiliation":[{"name":"Department of Computational Biomedicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8492-4187","authenticated-orcid":true,"given":"Hadijat-Kubura Moradeke","family":"Makinde","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Rheumatology Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myungja","family":"Ro","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, Allergy and Immunology, University of California, San Diego, La Jolla, CA 92093, USA."},{"name":"Department of Medicine, Kao Autoimmunity Institute and Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, 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