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IL‐12, IL‐23, and IL‐27 enhance human β‐defensin‐2 production in human keratinocytes
Author(s) -
Kanda Naoko,
Watanabe Shinichi
Publication year - 2008
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200738051
Subject(s) - tyrosine phosphorylation , biology , stat1 , phosphorylation , interleukin , microbiology and biotechnology , defensin , interleukin 17 , stat3 , immunology , inflammation , cytokine , antimicrobial
Abstract IL‐12, IL‐23, and IL‐27, which are produced by APC, modulate innate and adaptive immunities. Human β‐defensin‐2 (hBD‐2) produced by epidermal keratinocytes promotes cutaneous antimicrobial defense and inflammation. We examined the in vitro effects of IL‐12, IL‐23, and IL‐27 on hBD‐2 production in human keratinocytes. IL‐12, IL‐23, and IL‐27 enhanced IL‐1β‐induced hBD‐2 secretion and mRNA expression in keratinocytes. The stimulatory effects of IL‐12, IL‐23, and IL‐27 were suppressed by antisense oligonucleotides against NF‐κB p50 and p65. In addition, the effects of IL‐12 and IL‐27 were suppressed by antisense STAT3 and STAT1, respectively. All the three IL enhanced the basal and IL‐1β‐induced transcriptional activities of NF‐κB, while IL‐12 and IL‐27 enhanced STAT3 and STAT1 activities, respectively. Further, IL‐12, IL‐23, and IL‐27 promoted basal and IL‐1β‐induced phosphorylation of IκBα. IL‐12 and IL‐23 tyrosine phosphorylated STAT3 and STAT1, respectively; IL‐12, IL‐23, and IL‐27 tyrosine phosphorylated JAK2 and tyrosine kinase‐2; and IL‐27 tyrosine phosphorylated JAK1. These results suggest that IL‐12, IL‐23, and IL‐27 may enhance IL‐1β‐induced hBD‐2 production in keratinocytes by activating NF‐κB. STAT3 and STAT1 are involved in the effects of IL‐12 and IL‐27, respectively. Thus, IL‐12, IL‐23, and IL‐27 may promote cutaneous antimicrobial defense and inflammation via hBD‐2.