Immune Cell Function and Interaction
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A protective mechanism by which mucosal-associated invariant T (MAIT) cells detect microbiota metabolites produced upon intestinal inflammation and promote tissue repair is described, which is sensitive to a bacterial metabolic pathway indicative of intestinal inflammation.
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Intestinal inflammation shifts microbiota composition and metabolism. How the host monitors and responds to such changes remains unclear. Here, we describe a protective mechanism by which mucosal-associated invariant T (MAIT) cells detect microbiota metabolites produced upon intestinal inflammation and promote tissue repair. At steady state, MAIT ligands derived from the riboflavin biosynthesis pathway were produced by aerotolerant bacteria residing in the colonic mucosa. Experimental colitis triggered luminal expansion of riboflavin-producing bacteria, leading to increased production of MAIT ligands. Modulation of intestinal oxygen levels suggested a role for oxygen in inducing MAIT ligand production. MAIT ligands produced in the colon rapidly crossed the intestinal barrier and activated MAIT cells, which expressed tissue-repair genes and produced barrier-promoting mediators during colitis. Mice lacking MAIT cells were more susceptible to colitis and colitis-driven colorectal cancer. Thus, MAIT cells are sensitive to a bacterial metabolic pathway indicative of intestinal inflammation.
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@article{Morr2024MAIT,
title = {MAIT cells monitor intestinal dysbiosis and contribute to host protection during colitis},
author = {Yara El Morr and Mariela Fürstenheim and Martin Mestdagh and Katarzyna Franciszkiewicz and Marion Salou and Claire Morvan and Thierry Dupré and Alexey Vorobev and Bakhos Jneid and Virginie Prémel and Aurélie Darbois and Laëtitia Perrin and Stanislas Mondot and Ludovic Colombeau and Hélène Bugaut and Anastasia du Halgouet and Sophie Richon and Emanuele Procopio and Mathieu Maurin and Catherine Philippe and Raphaël Rodriguez and Olivier Lantz and François Legoux},
journal = {Science Immunology},
year = {2024},
doi = {10.1126/sciimmunol.adi8954},
url = {https://doi.org/10.1126/sciimmunol.adi8954}
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