{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T18:09:18Z","timestamp":1788804558005,"version":"build-2803163510"},"reference-count":75,"publisher":"American Society for Clinical Investigation","issue":"17","license":[{"start":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T00:00:00Z","timestamp":1788825600000},"content-version":"vor","delay-in-days":47,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Institutional funds","award":["Not applicable"],"award-info":[{"award-number":["Not applicable"]}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 AR071369"],"award-info":[{"award-number":["R01 AR071369"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 AR071369"],"award-info":[{"award-number":["R01 AR071369"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,8]]},"abstract":"<jats:p>\n                    The precise mechanisms underlying the pathogenesis of idiopathic inflammatory myopathy (IIM) remain undefined. However, there has been increasing recognition that tissue-resident memory T cells (TRMs) play an important role in the pathogenesis of systemic autoimmune disease. In IIM, TRM-associated transcriptional signatures have been reported but on a very limited basis. By using multimodal single-cell RNA-sequencing analysis in our established murine model of histidyl-tRNA synthetase\u2013induced myositis, we identified a prominent population of CD4\n                    <jats:sup>+<\/jats:sup>\n                    TRMs in inflamed skeletal muscle. Muscle CD4\n                    <jats:sup>+<\/jats:sup>\n                    TRMs exhibited high expression of genes encoding\n                    <jats:italic>Cd69<\/jats:italic>\n                    ,\n                    <jats:italic>Cxcr6<\/jats:italic>\n                    ,\n                    <jats:italic>Runx3<\/jats:italic>\n                    , and\n                    <jats:italic>Prdm1<\/jats:italic>\n                    , alongside low expression of\n                    <jats:italic>Klf2<\/jats:italic>\n                    ,\n                    <jats:italic>Ccr7<\/jats:italic>\n                    ,\n                    <jats:italic>Sell<\/jats:italic>\n                    ,\n                    <jats:italic>S1pr1<\/jats:italic>\n                    , and\n                    <jats:italic>Tcf7<\/jats:italic>\n                    \u2014 a profile that is generally consistent with previous reports of TRM gene signature and that we validate through comparison with transcriptomic profiles of human muscle tissue. Detailed pathway analysis in our model indicates that muscle CD4\n                    <jats:sup>+<\/jats:sup>\n                    TRMs contribute to innate immune regulatory pathways enriched for TNF and IFN-\u03b3 signaling. Furthermore, analysis of TCR clonotype distribution and CDR3 sequence similarity revealed pronounced clonal expansion of CD4\n                    <jats:sup>+<\/jats:sup>\n                    TRMs relative to other T cell subsets \u2014 a pattern that remained stable from 2 to 6 weeks after immunization. Collectively, these results suggest a potential role for CD4\n                    <jats:sup>+<\/jats:sup>\n                    TRMs in the pathogenesis of autoimmune myositis.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.208009","type":"journal-article","created":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T16:00:57Z","timestamp":1784822457000},"source":"Crossref","is-referenced-by-count":0,"title":["Single-cell RNA sequencing reveals clonally expanded CD4+ tissue-resident memory T cells in histidyl-tRNA synthetase\u2013induced myositis"],"prefix":"10.1172","volume":"11","author":[{"given":"Decheng","family":"Li","sequence":"first","affiliation":[{"name":"Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA."},{"name":"Tsinghua Medicine, Tsinghua University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel 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