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

Jan-Hendrik Schroeder1, Katrin Meissl2, Dominika Hromadová2

  • 1School of Immunology and Microbial Sciences, King's College London, London, United Kingdom.

Frontiers in Immunology
|February 19, 2021
PubMed
Summary
This summary is machine-generated.

T-bet deficiency increases innate lymphoid cell 3 (ILC3) numbers in mice, but does not cause inflammatory bowel disease. T-bet influences ILC3 populations, with precursors found within ILC3s.

Keywords:
ILCsT-betinnate lymphoid cellsintestinal inflammationmucosal homeostasis

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Innate lymphoid cells (ILCs) are crucial at mucosal surfaces.
  • T-bet-expressing ILC1s are implicated in inflammatory bowel disease (IBD).
  • The role of T-bet-negative ILC3s in colitis is debated.

Purpose of the Study:

  • To investigate the role of T-bet in ILC3 regulation and IBD pathogenesis.
  • To determine if T-bet deficiency impacts ILC3 cellularity and function.
  • To identify potential T-bet-expressing precursors within ILC3 populations.

Main Methods:

  • Analysis of T-bet deficient mice.
  • Flow cytometry to assess ILC populations (NKp46, RORγt, IL-7R).
  • In vivo fate-mapping to track T-bet+ precursors.

Main Results:

  • T-bet deficiency led to increased NKp46-negative ILC3s with enhanced RORγt and IL-7R expression.
  • STAT1 and STAT4 signaling were not involved in this regulation.
  • Enhanced neutrophilia was observed in colonic lamina propria, but no spontaneous colitis developed.
  • T-bet+ precursors were identified within NKp46-negative ILC3s.

Conclusions:

  • T-bet regulates ILC3 cellularity independently of STAT1/STAT4.
  • T-bet deficiency does not confer a higher risk for spontaneous colitis in SPF mice.
  • ILC3s can contain T-bet-expressing precursors, suggesting plasticity within ILC subsets.