{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T10:46:00Z","timestamp":1793702760644,"version":"4.5.1"},"reference-count":139,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,8,10]],"date-time":"2022-08-10T00:00:00Z","timestamp":1660089600000},"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>Systemic lupus erythematosus (SLE) is a typical autoimmune disease with a complex pathogenesis and genetic predisposition. With continued understanding of this disease, it was found that SLE is related to the interferon gene signature. Most studies have emphasized the important role of IFN-\u03b1 in SLE, but our previous study suggested a nonnegligible role of IFN-\u03b3 in SLE. Some scholars previously found that IFN-\u03b3 is abnormally elevated as early as before the classification of SLE and before the emergence of autoantibodies and IFN-\u03b1. Due to the large overlap between IFN-\u03b1 and IFN-\u03b3, SLE is mostly characterized by expression of the IFN-\u03b1 gene after onset. Therefore, the role of IFN-\u03b3 in SLE may be underestimated. This article mainly reviews the role of IFN-\u03b3 in SLE and focuses on the nonnegligible role of IFN-\u03b3 in SLE to gain a more comprehensive understanding of the disease.<\/jats:p>","DOI":"10.3389\/fimmu.2022.954706","type":"journal-article","created":{"date-parts":[[2022,8,10]],"date-time":"2022-08-10T03:12:53Z","timestamp":1660101173000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":88,"title":["IFN-\u03b3, should not be ignored in 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