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

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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.
Immunity ( IF 25.5 ) Pub Date : 2018-12-11 , DOI: 10.1016/j.immuni.2018.10.014
Jim G Castellanos ₁ , Viola Woo ₁ , Monica Viladomiu ₁ , Gregory Putzel ₁ , Svetlana Lima ₁ , Gretchen E Diehl ₂ , Andrew R Marderstein ₁ , Jorge Gandara ₁ , Alexendar R Perez ₁ , David R Withers ₃ , Stephan R Targan ₄ , David Q Shih ₄ , Ellen J Scherl ₅ , Randy S Longman ₆

Affiliation

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.

更新日期：2018-12-11

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