title: Induction of Interleukin-22 (IL-22) production in CD4+T Cells by IL-17A Secreted from CpG-Stimulated Keratinocytes.
abstract: BACKGROUND
  Interleukin-17A (IL-17A) is mainly secreted from Th17 cells that are activated by various stimuli including CpG oligodeoxynucleotide, a Toll-like receptor 9 (TLR9) ligand. Recently, it has been demonstrated that keratinocytes play an important role in the pathogenesis of psoriasis.
  
  
  OBJECTIVE
  To investigate the potential role of keratinocytes, we examined whether TLR9 ligand CpG induces IL-17A expression in keratinocytes.
  
  
  METHODS
  We used HaCaT keratinocytes as a model system, and determined CpG-induced IL-17A using enzyme-linked immunosorbent assay and Western blot.
  
  
  RESULTS
  When HaCaT keratinocytes were treated with CpG, the expression of several cytokines including IL-17A, tumor necrosis factor-α and CCL20 was markedly increased. Treatment with nuclear factor (NF)-κB inhibitor significantly blocked the CpG-induced IL-17A production, indicating that CpG induced IL-17A expression through the NF-κB signaling pathway. In addition, IL-17A secreted from keratinocytes stimulated the CD4+T cells, resulting in strong induction of IL-22 production.
  
  
  CONCLUSIONS
  Since IL-22 is an important mediator for psoriatic inflammation, our data suggest that keratinocytes can participate in the pathogenesis of psoriasis via the TLR9-dependent IL-17A production.
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Zheng Jun
authors.initials: ZJ
authors.lastname: Li
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Dae-Kyoung
authors.initials: DK
authors.lastname: Choi
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Kyung-Cheol
authors.initials: KC
authors.lastname: Sohn
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Seul Ki
authors.initials: SK
authors.lastname: Lim
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Myung
authors.initials: M
authors.lastname: Im
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Young
authors.initials: Y
authors.lastname: Lee
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Young-Joon
authors.initials: YJ
authors.lastname: Seo
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Chang Deok
authors.initials: CD
authors.lastname: Kim
authors.affiliation: Department of Dermatology, Chungnam National University School of Medicine, Daejeon, Korea.
authors.forename: Jeung-Hoon
authors.initials: JH
authors.lastname: Lee
keywords: CpG; Interleukin-17A; Keratinocytes; NF-κB; Psoriasis