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Microbiota-Induced TNF-like Ligand 1A Drives Group 3 Innate Lymphoid Cell-Mediated Barrier Protection and Intestinal T Cell Activation during Colitis.

Abstract：

:Inflammatory bowel disease (IBD) results from a dysregulated interaction between the microbiota and a genetically susceptible host. Genetic studies have linked TNFSF15 polymorphisms and its protein TNF-like ligand 1A (TL1A) with IBD, but the functional role of TL1A is not known. Here, we found that adherent IBD-associated microbiota induced TL1A release from CX3CR1+ mononuclear phagocytes (MNPs). Using cell-specific genetic deletion models, we identified an essential role for CX3CR1+MNP-derived TL1A in driving group 3 innate lymphoid cell (ILC3) production of interleukin-22 and mucosal healing during acute colitis. In contrast to this protective role in acute colitis, TL1A-dependent expression of co-stimulatory molecule OX40L in MHCII+ ILC3s during colitis led to co-stimulation of antigen-specific T cells that was required for chronic T cell colitis. These results identify a role for ILC3s in activating intestinal T cells and reveal a central role for TL1A in promoting ILC3 barrier immunity during colitis.

journal_name

Immunity

journal_title

Immunity

authors

Castellanos JG,Woo V,Viladomiu M,Putzel G,Lima S,Diehl GE,Marderstein AR,Gandara J,Perez AR,Withers DR,Targan SR,Shih DQ,Scherl EJ,Longman RS

doi

10.1016/j.immuni.2018.10.014

subject

Has Abstract

pub_date

2018-12-18 00:00:00

pages

1077-1089.e5

issue

6

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(18)30479-5

journal_volume

49

pub_type

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