Type I IFNs at the interface between cutaneous immunity and epidermal remodeling.
Type I IFNs are key cytokines in antiviral host defense. Preferentially expressed by plasmacytoid dendritic cells, type I IFNs are induced by viral infection and in common skin wounds. In this issue, Tohyama et al. identify a new link between type I IFNs and epidermal remodeling, by showing that type I IFNs specifically upregulate IL-22R expression on keratinocytes and, thereby, IL-22-mediated Stat3 phosphorylation in keratinocytes. The findings suggest that type I IFNs play dual roles in human skin: first, they induce immune activation with the induction of IL-22-producing T cells; second, they provide the interface between immune activation and epidermal remodeling by increasing keratinocyte responsiveness to IL-22.
Department of Dermatology, Lausanne University Hospital of Lausanne, Lausanne, Switzerland.
Curdin
C
Conrad
Michel
M
Gilliet
D006801:Humans; D016898:Interferon-alpha / Q000494:pharmacology*; D015603:Keratinocytes / Q000187:drug effects*; D011565:Psoriasis / Q000209:etiology*; D018123:Receptors, Interleukin / Q000235:genetics*
D016898:Interferon-alpha; D018123:Receptors, Interleukin; C415369:interleukin-22 receptor