Dysregulated balance of retinoid-related orphan receptor γt-dependent innate lymphoid cells is involved in the pathogenesis of chronic DSS-induced colitis

Kayoko Kimura, Takanori Kanai, Atsushi Hayashi, Yohei Mikami, Tomohisa Sujino, Shinta Mizuno, Tango Handa, Katsuyoshi Matsuoka, Tadakazu Hisamatsu, Toshiro Sato, Toshifumi Hibi

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Retinoid-related orphan receptor (ROR) γt-expressing and IL-22-producing NKp46+ innate lymphoid (ILC22) cells reside in the lamina propria of the intestine in mice, suggesting that ILC22 cells contribute to host defense during intestinal damage in models of colitis in mice. Nevertheless, another set of pathological interferon (IFN)-γ and/or IL-17A-producing innate lymphoid cells (ILC1 and ICL17) may participate in the pathogenesis in different models of colitis. We here showed that RORγt+IL-22+ ILC22 cells were localized in Thy-1highSCA-1high and/or Thy-1highSCA-1low subpopulations of the intestine in normal and dextran sodium sulfate (DSS)-induced colitic RORγt-sufficient Rag-2-/- mice. RORγt-deficient Rag-2-/- mice developed more severe DSS-induced colitis accompanied with lower expression of REG3β and REG3γ in the colon, but with a lower ratio and absolute number of IFN-γ-producing ILC1 cells as compared to control RORγt-sufficient Rag-2-/- mice. Collectively, not only the presence of ILC22 cells but also the balance of protective and pathogenic ILCs may be involved in the prevention of colitis.

Original languageEnglish
Pages (from-to)694-700
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume427
Issue number4
DOIs
Publication statusPublished - 2012 Nov 2

Keywords

  • Chronic colitis
  • IL-22
  • Innate lymphoid cells
  • RORγt

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Dysregulated balance of retinoid-related orphan receptor γt-dependent innate lymphoid cells is involved in the pathogenesis of chronic DSS-induced colitis'. Together they form a unique fingerprint.

Cite this