Th17 cells carrying TCR recognizing epidermal autoantigen induce psoriasis-like skin inflammation

Shuhei Nishimoto, Hitoshi Kotani, Sanae Tsuruta, Nana Shimizu, Minako Ito, Takashi Shichita, Rimpei Morita, Hayato Takahashi, Masayuki Amagai, Akihiko Yoshimura

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Psoriasis is considered a Th17-type autoimmune skin inflammatory disease; however, involvement of an autoantigen-specific TCR has not been established. In this study, we show that psoriasis-like skin inflammation can be induced by autoreactive Th17 cells.We previously developed the desmoglein 3-specific TCR-transgenic (Dsg3H1) mouse, in which CD4+ T cells recognize physiological epidermal autoantigen. T cells from Dsg3H1 mice were polarized into Th17 cells in vitro and then adoptively transferred into Rag2-/- mice. Dsg3H1-Th17 cells induced severe psoriasis-like skin inflammation within 2 wk after transfer in the tissues in which desmoglein 3 is expressed. Such pathology was not observed when wild-type Th17 cells or Th1-skewed Dsg3H1 T cells were transferred, and it was strongly suppressed by anti-IL-12/23 and anti-IL-17 Abs. Although IFN-γ+/IL-17+ T cells accumulated in the skin lesions of mice that received Dsg3H1-Th17 cells, IFN-γ-deficient Dsg3H1-Th17 cells were fully pathogenic. These results demonstrate that cutaneous psoriasis-like immunopathology can be developed by epidermis-specific recognition of Th17 cells, which is strictly dependent on IL-17 but not IFN-γ.

Original languageEnglish
Pages (from-to)3065-3072
Number of pages8
JournalJournal of Immunology
Volume191
Issue number6
DOIs
Publication statusPublished - 2013 Sep 15

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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