Enrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis

Emi Irie, Rino Ishihara, Ichiro Mizushima, Shunya Hatai, Yuya Hagihara, Yoshiaki Takada, Junya Tsunoda, Kentaro Iwata, Yuta Matsubara, Yusuke Yoshimatsu, Hiroki Kiyohara, Nobuhito Taniki, Tomohisa Sujino, Kaoru Takabayashi, Naoki Hosoe, Haruhiko Ogata, Toshiaki Teratani, Nobuhiro Nakamoto, Yohei Mikami, Takanori Kanai

研究成果: Article査読


Group 2 innate lymphoid cells (ILC2s) serve as frontline defenses against parasites. However, excluding helminth infections, it is poorly understood how ILC2s function in intestinal inflammation, including inflammatory bowel disease. Here, we analyzed the global gene expression of ILC2s in healthy and colitic conditions and revealed that type I interferon (T1IFN)-stimulated genes were up-regulated in ILC2s in dextran sodium sulfate (DSS)-induced colitis. The enhancement of T1IFN signaling in ILC2s in DSS-induced colitis was correlated with the downregulation of cytokine production by ILC2s, such as interleukin-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis in both wild-type and Rag2-deficient mice. The exacerbation of colitis induced by neutralization of T1IFN signaling was accompanied by reduction of amphiregulin (AREG) in ILC2s and was partially rescued by exogenous AREG treatment. Collectively, these findings show the potential roles of T1IFN in ILC2s that contribute to colitis manifestation.

ジャーナルFrontiers in Immunology
出版ステータスPublished - 2022 10月 4

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学


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