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Immunity. 2011 Oct 28;35(4):596-610. doi: 10.1016/j.immuni.2011.08.001. Epub 2011 Oct 6.

Pivotal role of dermal IL-17-producing γδ T cells in skin inflammation.

Author information

  • 1Department of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 20025, PR China.

Erratum in

  • Immunity. 2011 Oct 28;35(4):649.

Abstract

Interleukin-23 (IL-23) and CD4(+) T helper 17 (Th17) cells are thought to be critical in psoriasis pathogenesis. Here, we report that IL-23 predominantly stimulated dermal γδ T cells to produce IL-17 that led to disease progression. Dermal γδ T cells constitutively expressed the IL-23 receptor (IL-23R) and transcriptional factor RORγt. IL-17 production from dermal γδ T cells was independent of αβ T cells. The epidermal hyperplasia and inflammation induced by IL-23 were significantly decreased in T cell receptor δ-deficient (Tcrd(-/-)) and IL-17 receptor-deficient (Il17ra(-/-)) mice but occurred normally in Tcra(-/-) mice. Imiquimod-induced skin pathology was also significantly decreased in Tcrd(-/-) mice. Perhaps further promoting disease progression, IL-23 stimulated dermal γδ T cell expansion. In psoriasis patients, γδ T cells were greatly increased in affected skin and produced large amounts of IL-17. Thus, IL-23-responsive dermal γδ T cells are the major IL-17 producers in the skin and may represent a novel target for the treatment of psoriasis.

Copyright © 2011 Elsevier Inc. All rights reserved.

Comment in

  • Inflammation: Under the skin. [Nat Rev Immunol. 2011]
PMID:
21982596
[PubMed - indexed for MEDLINE]
PMCID:
PMC3205267
Free PMC Article

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