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PMID:16982811

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Citation

Liang, SC, Tan, XY, Luxenberg, DP, Karim, R, Dunussi-Joannopoulos, K, Collins, M and Fouser, LA (2006) Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides. J. Exp. Med. 203:2271-9

Abstract

Th17 cells are a distinct lineage of effector CD4(+) T cells characterized by their production of interleukin (IL)-17. We demonstrate that Th17 cells also expressed IL-22, an IL-10 family member, at substantially higher amounts than T helper (Th)1 or Th2 cells. Similar to IL-17A, IL-22 expression was initiated by transforming growth factor beta signaling in the context of IL-6 and other proinflammatory cytokines. The subsequent expansion of IL-22-producing cells was dependent on IL-23. We further demonstrate that IL-22 was coexpressed in vitro and in vivo with both IL-17A and IL-17F. To study a functional relationship among these cytokines, we examined the expression of antimicrobial peptides by primary keratinocytes treated with combinations of IL-22, IL-17A, and IL-17F. IL-22 in conjunction with IL-17A or IL-17F synergistically induced the expression of beta-defensin 2 and S100A9 and additively enhanced the expression of S100A7 and S100A8. Collectively, we have identified IL-22 as a new cytokine expressed by Th17 cells that synergizes with IL-17A or IL-17F to regulate genes associated with skin innate immunity.

Links

PubMed PMC2118116 Online version:10.1084/jem.20061308

Keywords

Animals; Antimicrobial Cationic Peptides/immunology; Antimicrobial Cationic Peptides/metabolism; CD4-Positive T-Lymphocytes/immunology; Cell Differentiation/immunology; Immunity, Innate/immunology; Interleukin-17/genetics; Interleukin-17/immunology; Interleukins/genetics; Interleukins/immunology; Keratinocytes/metabolism; Mice; Mice, Transgenic; Polymerase Chain Reaction; Signal Transduction/immunology; Transforming Growth Factor beta/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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