A recent study by Cohen et al. identified stress-induced keratin 16 (KRT16) as an active regulator of skin innate immunity. By sequestering 14-3-3ε, KRT16 suppresses retinoic acid-inducible gene I-mediated type I interferon (IFN) signalling. KRT16 loss in pachyonychia congenita amplifies inflammatory IFN signalling, highlighting the KRT16-IFN signalling axis as a potential therapeutic target.
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Shah et al. (2026) studied this question.
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