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Transl. Med."],"published-print":{"date-parts":[[2026,4,8]]},"abstract":"<jats:p>\n                    The stress-induced keratin 16 intermediate filament gene,\n                    <jats:italic toggle=\"yes\">KRT16<\/jats:italic>\n                    , and K16 protein are spatially restricted to the suprabasal layers of the epidermis and widely used as biomarkers in psoriasis, hidradenitis suppurativa, atopic dermatitis, and other inflammatory disorders. Pathogenic variants in\n                    <jats:italic toggle=\"yes\">KRT16<\/jats:italic>\n                    cause pachyonychia congenita (PC), a rare genetic condition in which tissue homeostasis is disrupted in palmoplantar epidermis, nail, oral mucosa, and other\n                    <jats:italic toggle=\"yes\">KRT16<\/jats:italic>\n                    -expressing epithelial appendages. How K16 may regulate the molecular mechanisms underlying these conditions is poorly understood. Here, we show that K16 negatively regulates type I interferon (IFN) signaling and innate immune responses in skin. Clinically, the signature palmoplantar keratoderma lesions in individuals with PC showed enhanced type I IFN signaling. In mouse skin in vivo, loss of\n                    <jats:italic toggle=\"yes\">Krt16<\/jats:italic>\n                    led to exacerbation of imiquimod-induced psoriasiform disease and heightened recruitment of neutrophils in a phorbol ester\u2013induced model of acute sterile inflammation. In\n                    <jats:italic toggle=\"yes\">KRT16<\/jats:italic>\n                    -null human keratinocytes, loss of K16 amplified IFN signaling including phosphorylated interferon regulatory factor 7 (IRF7) and interferon-stimulated gene 15 (ISG15) after treatment with synthetic dsRNA poly(I:C). Mechanistically, K16 interacted with effectors of the RIG-I\u2013like receptor (RLR) pathway, including 14-3-3\u025b, and inhibited the 14-3-3\u025b:RIG-I interaction upstream of IFN activation in mouse and immortalized human keratinocytes ex vivo. Topical application of the Janus kinase inhibitor cream ruxolitinib to palmoplantar keratoderma lesions of\n                    <jats:italic toggle=\"yes\">Krt16<\/jats:italic>\n                    -null mice reduced lesion severity. These findings uncover a previously unrecognized paradigm for keratin-dependent regulation of innate immunity, with implications for our understanding of inflammatory skin diseases and potential treatments for PC.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx9123","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T17:59:41Z","timestamp":1775671181000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":4,"title":["Keratin 16 inhibits type I interferon responses in differentiating keratinocytes of stressed and diseased skin"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2390-3707","authenticated-orcid":true,"given":"Erez","family":"Cohen","sequence":"first","affiliation":[{"name":"Department of Cell &amp; Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5398-087X","authenticated-orcid":true,"given":"Yang","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonal","family":"Ghodke","sequence":"additional","affiliation":[{"name":"Department of Cell &amp; 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Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3943-5891","authenticated-orcid":true,"given":"Kaylee","family":"Steen","sequence":"additional","affiliation":[{"name":"Department of Cell &amp; Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8505-4259","authenticated-orcid":true,"given":"Mrinal K.","family":"Sarkar","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5157-8780","authenticated-orcid":true,"given":"Nurhan","family":"\u00d6zl\u00fc","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Genetics, Science Faculty, Ko\u00e7 University, Istanbul, 34450, Turkey."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1627-5722","authenticated-orcid":true,"given":"Lam C.","family":"Tsoi","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0080-0812","authenticated-orcid":true,"given":"Johann E.","family":"Gudjonsson","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9980-6308","authenticated-orcid":true,"given":"Lucile","family":"Marchal","sequence":"additional","affiliation":[{"name":"Institut Imagine - Inserm U1163, 75015 Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3412-7512","authenticated-orcid":true,"given":"Alain","family":"Hovnanian","sequence":"additional","affiliation":[{"name":"Institut Imagine - Inserm U1163, 75015 Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1518-1452","authenticated-orcid":true,"given":"Carole A.","family":"Parent","sequence":"additional","affiliation":[{"name":"Department of Cell &amp; 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