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Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation.

Abstract：

:TNF-like ligand 1 A (TL1A) and death receptor 3 (DR3) are a ligand-receptor pair involved in the pathogenesis of inflammatory bowel disease. Group 3 innate lymphoid cells (ILC3s) regulate intestinal immunity and highly express DR3. Here, we report that activation of DR3 signaling by an agonistic anti-DR3 antibody increases GM-CSF production from ILC3s through the p38 MAPK pathway. GM-CSF causes accumulation of eosinophils, neutrophils and CD11b+CD11c+ myeloid cells, resulting in loss of ILC3s from the intestine in an IL-23-dependent manner and exacerbating colitis. Blockade of GM-CSF or IL-23 reverses anti-DR3 antibody-driven ILC3 loss, whereas overexpression of IL-23 induces loss of ILC3s in the absence of GM-CSF. Neutralization of TL1A by soluble DR3 ameliorates both DSS and anti-CD40 antibody-induced colitis. Moreover, ILC3s are required for the deleterious effect of anti-DR3 antibodies on innate colitis. These findings clarify the process and consequences of DR3 signaling-induced intestinal inflammation through regulation of ILC3s.

journal_name

Nat Commun

journal_title

Nature communications

authors

Li J,Shi W,Sun H,Ji Y,Chen Y,Guo X,Sheng H,Shu J,Zhou L,Cai T,Qiu J

doi

10.1038/s41467-019-11304-8

subject

Has Abstract

pub_date

2019-07-29 00:00:00

pages

3371

issue

1

issn

2041-1723

pii

10.1038/s41467-019-11304-8

journal_volume

10

pub_type

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