Journal
IMMUNITY
Volume 55, Issue 3, Pages 494-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2022.02.003
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Funding
- NIH
- Crohn's and Colitis Foundation
- NIH/NIAID
- UAB Training Program in Immunologic Diseases and Basic Immunology
- UAB MSTP training grant funds
- NIH/NIDDK
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IL-22 produced by ILCs and T cells plays different roles in immune defense against Citrobacter rodentium infection. ILC-derived IL-22 temporarily restrains bacterial growth, while T cell-derived IL-22 protects the intestinal crypts by inducing a host-protective transcriptomic program.
Interleukin (IL)-22 is central to immune defense at barrier sites. We examined the contributions of innate lymphoid cell (ILC) and T cell-derived IL-22 during Citrobacter rodentium (C.r) infection using mice that both report Il22 expression and allow lineage-specific deletion. ILC-derived IL-22 activated STAT3 in C.r-colonized surface intestinal epithelial cells (IECs) but only temporally restrained bacterial growth. T cell-derived IL-22 induced a more robust and extensive activation of STAT3 in IECs, including IECs lining colonic crypts, and T cell-specific deficiency of IL-22 led to pathogen invasion of the crypts and increased mortality. This reflected a requirement for T cell-derived IL-22 for the expression of a host-protective transcriptomic program that included AMPs, neutrophil-recruiting chemokines, and mucin-related molecules, and it restricted IFNg-induced proinflammatory genes. Our findings demonstrate spatiotemporal differences in the production and action of IL-22 by ILCs and T cells during infection and reveal an indispensable role for IL-22-producing T cells in the protection of the intestinal crypts.
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