{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T05:41:29Z","timestamp":1793166089706,"version":"4.5.0"},"reference-count":74,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"817","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2025,9,24]]},"abstract":"<jats:p>\n            Rheumatoid arthritis (RA) is preceded by an at-risk stage of disease that can be marked by the presence of anticitrullinated protein antibodies (ACPAs) but the absence of clinically apparent synovitis (clinical RA). Preemptive intervention in at-risk individuals could prevent or delay future tissue damage; however, the immunobiology of this stage is unclear. Using integrative multiomics, we longitudinally profiled at-risk individuals, where one-third of participants developed clinical RA on study. We found evidence of systemic inflammation and signatures of activation in na\u00efve T and B cells of at-risk individuals. During progression to clinical RA, proinflammatory skewing of atypical B cells and expansion of memory CD4 T cells with signatures of activation and B cell help were present without elevations in circulating ACPA titers. Epigenetic changes in na\u00efve CD4 T cells suggested a predisposition to differentiate into effector cells capable of B cell help. These findings characterize pathogenesis of the ACPA\n            <jats:sup>+<\/jats:sup>\n            at-risk stage and support the concept that the disease begins much earlier than clinical RA. Additionally, an extensive immune resource of the at-risk stage and progression to clinical RA with interactive tools was developed to enable further investigation.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.adt7214","type":"journal-article","created":{"date-parts":[[2025,9,24]],"date-time":"2025-09-24T17:58:12Z","timestamp":1758736692000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":32,"title":["Progression to rheumatoid arthritis in at-risk individuals is defined by systemic inflammation and by T and B cell dysregulation"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3556-8248","authenticated-orcid":true,"given":"Ziyuan","family":"He","sequence":"first","affiliation":[{"name":"Allen Institute for Immunology, Seattle, WA 98109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3763-0842","authenticated-orcid":true,"given":"Marla C.","family":"Glass","sequence":"additional","affiliation":[{"name":"Allen Institute for Immunology, Seattle, WA 98109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pravina","family":"Venkatesan","sequence":"additional","affiliation":[{"name":"Allen Institute for Immunology, Seattle, WA 98109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-0598-853X","authenticated-orcid":true,"given":"Marie L.","family":"Feser","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Aurora CO 80045, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-8075-9062","authenticated-orcid":true,"given":"Leander","family":"Lazaro","sequence":"additional","affiliation":[{"name":"University of California, San Diego, San Diego, CA 92093, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5691-3373","authenticated-orcid":true,"given":"Lauren Y.","family":"Okada","sequence":"additional","affiliation":[{"name":"Allen Institute for Immunology, Seattle, WA 98109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9660-8904","authenticated-orcid":true,"given":"Nhung T. 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