{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T05:03:09Z","timestamp":1784782989623,"version":"3.55.0"},"reference-count":88,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T00:00:00Z","timestamp":1784764800000},"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>\n                    Interferon-\u03c9 (IFN-\u03c9) is a member of the human type I interferon family that has historically been overshadowed by IFN-\u03b1 and IFN-\u03b2. Recent human \u201cnatural perturbations\u201d, most notably selective neutralization of IFN-\u03c9 by autoantibodies in life-threatening viral infections, have renewed interest in this comparatively understudied cytokine and indicate that its antiviral activity may not always be fully compensated in defined clinical settings. This renewed focus has prompted reassessment of its single-gene organization, distinct antigenicity, intermediate receptor-binding kinetics, cellular sources, and regulatory mechanisms. In parallel, thymus-centered tolerance disorders, including autoimmune regulator (\n                    <jats:italic>AIRE<\/jats:italic>\n                    ) deficiency, additional inborn errors of immune tolerance, and acquired \u201csick thymus\u201d states, establish anti-IFN-\u03c9 autoantibodies as a stable, high-penetrance immunophenotype linking tolerance failure to durable cytokine-directed autoimmunity. Beyond antiviral defense, multi-omic studies in lupus-spectrum disease suggest tissue- and compartment-specific IFN-\u03c9 signals within broader type I interferon programs, yet endogenous IFN-\u03c9 remains rarely quantified with ligand-level resolution. This Review integrates current knowledge of IFN-\u03c9 from molecular regulation to human disease. Further progress will require subtype-resolved measurement, direct comparison with other type I interferons under matched conditions, and human genetic studies testing whether rare\n                    <jats:italic>IFNW1<\/jats:italic>\n                    variants contribute to severe viral disease.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1891351","type":"journal-article","created":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T04:29:59Z","timestamp":1784780999000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Human interferon-\u03c9: an underappreciated type I interferon"],"prefix":"10.3389","volume":"17","author":[{"given":"Ruyue","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Nephrology and Immunology, Children\u2019s Hospital of Soochow University","place":["Suzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,23]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1098\/rspb.1957.0048","article-title":"Virus interference. 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