Journal
GUT MICROBES
Volume 11, Issue 2, Pages 231-236Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/19490976.2019.1638725
Keywords
Innate lymphoid cells; inflammatory bowel diseases; TL1A; OX40L
Categories
Funding
- Crohn's and Colitis Foundation
- NIH [1R03DK111852, 1R01 DK114252]
- NIH Medical Scientist Training Program [T32GM07739]
- Charina Foundation
- Crohn's and Colitis Foundation of America
- National Institute of Diabetes and Digestive and Kidney Diseases [R01 DK114252, 1R03DK111852-01A1]
- Charina Endowment Fund
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Despite continuous exposure to trillions of microbes, the intestinal immune system protects the mucosa by balancing barrier protection, tolerance, and immunity. As both sentinel and effector, the mucosal innate immune system plays a central role in coordinating these responses. By integrating signals from the intestinal microbiota, mononuclear phagocytes (MNPs) serve as a critical link in regulating effector functions of group 3 innate lymphoid cells (ILC3s). Our recent work identified the role for MNP production of the IBD-linked protein TNF-like ligand 1A (TL1A) in modulating microbial regulation of ILC3 barrier immunity. These findings highlight a broader role for ILC3s in local control of T cell immunity and their potential role in the pathogenesis and treatment of inflammatory disease.
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