| First Author | Kimura K | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 427 |
| Issue | 4 | Pages | 694-700 |
| PubMed ID | 23022186 | Mgi Jnum | J:190311 |
| Mgi Id | MGI:5448585 | Doi | 10.1016/j.bbrc.2012.09.091 |
| Citation | Kimura K, et al. (2012) Dysregulated balance of retinoid-related orphan receptor gammat-dependent innate lymphoid cells is involved in the pathogenesis of chronic DSS-induced colitis. Biochem Biophys Res Commun 427(4):694-700 |
| abstractText | Retinoid-related orphan receptor (ROR) gammat-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)-gamma 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 RORgammat(+)IL-22(+) ILC22 cells were localized in Thy-1(high)SCA-1(high) and/or Thy-1(high)SCA-1(low) subpopulations of the intestine in normal and dextran sodium sulfate (DSS)-induced colitic RORgammat-sufficient Rag-2(-/-) mice. RORgammat-deficient Rag-2(-/-) mice developed more severe DSS-induced colitis accompanied with lower expression of REG3beta and REG3gamma in the colon, but with a lower ratio and absolute number of IFN-gamma-producing ILC1 cells as compared to control RORgammat-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. |
