期刊
FRONTIERS IN IMMUNOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.623324
关键词
T-bet; innate lymphoid cells; ILCs; intestinal inflammation; mucosal homeostasis
类别
资金
- Wellcome Trust [091009]
- Medical Research Council [MR/M003493/1, MR/K002996/1]
- National Institute for Health Research (NIHR) Biomedical Research Centre at Guy's and St Thomas and King's College London
- Austrian Science Fund [SFB-F6101]
- Welcome Trust [WT101159]
- NIHR Imperial Biomedical Research Center
- RCUK/UKRI Rutherford Fund fellowship [MR/R024812/1]
- MRC [MR/K002996/1, MR/R024812/1, MR/M003493/1] Funding Source: UKRI
T-bet deficient mice show an increase in ILC3 cellularity but do not have a greater risk of developing spontaneous colitis. T-bet appears to control the number of ILC3 cells, but does not drive a pathogenic role of ILC3 in mice with a conventional specific pathogen-free microbiota.
Innate lymphoid cells (ILC) play a significant immunological role at mucosal surfaces such as the intestine. T-bet-expressing group 1 innate lymphoid cells (ILC1) are believed to play a substantial role in inflammatory bowel disease (IBD). However, a role of T-bet-negative ILC3 in driving colitis has also been suggested in mouse models questioning T-bet as a critical factor for IBD. We report here that T-bet deficient mice had a greater cellularity of NKp46-negative ILC3 correlating with enhanced expression of ROR gamma t and IL-7R, but independent of signaling through STAT1 or STAT4. We observed enhanced neutrophilia in the colonic lamina propria (cLP) of these animals, however, we did not detect a greater risk of T-bet-deficient mice to develop spontaneous colitis. Furthermore, by utilizing an in vivo fate-mapping approach, we identified a population of T-bet-positive precursors in NKp46-negative ILC3s. These data suggest that T-bet controls ILC3 cellularity, but does do not drive a pathogenic role of ILC3 in mice with a conventional specific pathogen-free microbiota.
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