{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:11:10Z","timestamp":1791223870478,"version":"4.1.0"},"reference-count":101,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"778","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2024,12,18]]},"abstract":"<jats:p>\n            Sj\u00f6gren\u2019s disease (SjD) is an autoimmune disorder characterized by progressive salivary and lacrimal gland dysfunction, inflammation, and destruction, as well as extraglandular manifestations. SjD is associated with autoreactive B and T cells, but its pathophysiology remains incompletely understood. Abnormalities in regulatory T (T\n            <jats:sub>reg<\/jats:sub>\n            ) cells occur in several autoimmune diseases, but their role in SjD is ambiguous. We had previously shown that the function and development of T\n            <jats:sub>reg<\/jats:sub>\n            cells depend on store-operated Ca\n            <jats:sup>2+<\/jats:sup>\n            entry (SOCE), which is mediated by ORAI1 Ca\n            <jats:sup>2+<\/jats:sup>\n            channels and stromal interaction protein 1 (STIM1) and STIM2. Here, we show that mice with a Foxp3\n            <jats:sup>+<\/jats:sup>\n            T\n            <jats:sub>reg<\/jats:sub>\n            cell\u2013specific deletion of\n            <jats:italic>Stim1<\/jats:italic>\n            and\n            <jats:italic>Stim2<\/jats:italic>\n            develop a phenotype that fulfills all classification criteria of human SjD. Mutant mice have salivary and lacrimal gland inflammation characterized by strong lymphocyte infiltration and transcriptional signatures dominated by T helper 1 (T\n            <jats:sub>H<\/jats:sub>\n            1) and interferon (IFN) signaling. CD4\n            <jats:sup>+<\/jats:sup>\n            T cells from mutant mice are sufficient to induce SjD-like disease in an IFN-\u03b3\u2013dependent manner. Inhibition of IFN signaling with the JAK1\/2 inhibitor baricitinib alleviated CD4\n            <jats:sup>+<\/jats:sup>\n            T cell\u2013induced SjD in mice. These findings are consistent with the transcriptional profiles of CD4\n            <jats:sup>+<\/jats:sup>\n            T cells from patients with SjD, which indicate enhanced T\n            <jats:sub>H<\/jats:sub>\n            1 but reduced memory T\n            <jats:sub>reg<\/jats:sub>\n            cell function. Together, our study provides evidence for a critical role of dysfunctional T\n            <jats:sub>reg<\/jats:sub>\n            cells and IFN-\u03b3\u2013producing T\n            <jats:sub>H<\/jats:sub>\n            1 cells in the pathogenesis of SjD.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.ado4856","type":"journal-article","created":{"date-parts":[[2024,12,18]],"date-time":"2024-12-18T19:00:17Z","timestamp":1734548417000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":43,"title":["IFN-\u03b3\u2013producing T\n            <sub>H<\/sub>\n            1 cells and dysfunctional regulatory T cells contribute to the pathogenesis of Sj\u00f6gren\u2019s disease"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3637-8852","authenticated-orcid":true,"given":"Yin-Hu","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pathology, New York University Grossman School of 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