AUTHOR=Schroeder Jan-Hendrik , Meissl Katrin , Hromadová Dominika , Lo Jonathan W. , Neves Joana F. , Howard Jane K. , Helmby Helena , Powell Nick , Strobl Birgit , Lord Graham M. 

TITLE=T-Bet Controls Cellularity of Intestinal Group 3 Innate Lymphoid Cells

JOURNAL=Frontiers in Immunology

VOLUME=11

YEAR=2021

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.623324

DOI=10.3389/fimmu.2020.623324

ISSN=1664-3224

ABSTRACT=<p>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 RORγt 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 <italic>in vivo</italic> 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.</p>