CCR6 is required for epidermal trafficking of γδ-T cells in an IL-23-Induced model of psoriasiform dermatitis

Tomotaka Mabuchi, Tej Pratap Singh, Tomonori Takekoshi, Guang Fu Jia, Xuesong Wu, Mandy C. Kao, Ido Weiss, Joshua M. Farber, Samuel T Hwang

Research output: Contribution to journalArticlepeer-review

98 Scopus citations


A subset of CC chemokine receptor-6 + (CCR6 +), γδ-low (GDL) T cells that express Th17 cytokines in mouse skin participates in IL-23-induced psoriasiform dermatitis. We use CCR6-deficient (knockout, KO) and wild-type (WT) mice to analyze skin trafficking patterns of GDL T cells and function-blocking mAbs to determine the role of CCR6 in IL-23-mediated dermatitis. Herein, CCL20 was highly upregulated in IL-23-injected WT mouse ear skin as early as 24 hours after initial treatment, and large numbers of CCR6 + cells were observed in the epidermis of IL-23-injected WT mice. Anti-CCL20 mAbs reduced psoriasiform dermatitis and blocked recruitment of GDL T cells to the epidermis. In CCR6 KO mice, GDL T cells failed to accumulate in the epidermis after IL-23 treatment, but the total numbers of GDL T cells in the dermis of WT and CCR6 KO mice were equivalent. There was an ∼70% reduction in the proportion of IL-22 + GDL T cells in the dermis of CCR6 KO mice (vs WT mice), suggesting that effector function and epidermal recruitment of GDL T cells are impaired in CCR6-deficient mice. Thus, these data show that CCR6 regulates epidermal trafficking of γδ-T-cell subsets in the skin and suggest the potential of CCR6 as a therapeutic target for psoriasis.

Original languageEnglish (US)
Pages (from-to)164-171
Number of pages8
JournalJournal of Investigative Dermatology
Issue number1
StatePublished - Jan 2013
Externally publishedYes

ASJC Scopus subject areas

  • Dermatology
  • Biochemistry
  • Cell Biology
  • Molecular Biology


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