{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T14:48:54Z","timestamp":1789742934634,"version":"4.0.1"},"reference-count":152,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T00:00:00Z","timestamp":1764115200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Dysregulation of type I interferon (IFN-I) signaling has been implicated in the pathogenesis of multiple systemic autoimmune diseases, including systemic lupus erythematosus, Sj\u00f6gren\u2019s syndrome, and rheumatoid arthritis. Tripartite motif-containing protein 21 (TRIM21) serves as both a major autoantigen and a pivotal E3 ubiquitin ligase. In the IFN-I pathway, TRIM21 plays a dual regulatory role by targeting transcription factors such as interferon regulatory factor 3 (IRF3), interferon regulatory factor 5 (IRF5), and interferon regulatory factor 7 (IRF7) through multiple ubiquitination mechanisms. This duality enables TRIM21 to both activate IFN-I signaling and mediate its negative feedback, thus maintaining immune homeostasis. However, the presence of anti-TRIM21 autoantibodies may impair its ubiquitin ligase function, resulting in persistent activation of the IFN-I pathway and chronic inflammation. This review summarizes the mechanisms by which TRIM21 regulates IRF family members across various tissues and immune contexts, and explores how its dysfunction contributes to tissue-specific inflammatory responses. Furthermore, we evaluate the potential diagnostic and stratification value of anti-Ro52 antibodies and propose TRIM21 as a novel upstream therapeutic target to restore interferon balance in autoimmune diseases.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1695818","type":"journal-article","created":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T06:31:53Z","timestamp":1764138713000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["TRIM21 regulation of IRF-mediated type I interferon signaling in systemic autoimmune diseases"],"prefix":"10.3389","volume":"16","author":[{"given":"Kailai","family":"Panlu","sequence":"first","affiliation":[{"name":"The Second School of Clinical Medicine, Zhejiang Chinese Medical University","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yihan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, The Second 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