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Publié dans: 2021

Auteurs: Dan Corral, Alison Charton, Maria Z Krauss, Eve Blanquart, Florence Levillain, Emma Lefrançais, Tamara Sneperger, Jean-Philippe Girard, Gérard Eberl, Yannick Poquet, Jean-Charles Guéry, Rafael J Argüello, Matthew R Hepworth, Olivier Neyrolles, Denis Hudrisier

Résumé

Tissue-resident innate lymphoid cells (ILCs) regulate tissue homeostasis, protect against pathogens at mucosal surfaces and are key players at the interface of innate and adaptive immunity. How ILCs adapt their phenotype and function to environmental cues within tissues remains to be fully understood. Here, we show that Mycobacterium tuberculosis infection alters the phenotype and function of immature lung ILC2 toward a protective interferon-γ-producing ILC1-like population. This differentiation is controlled by type 1 cytokines and is associated with a glycolytic program involving the transcription factor HIF1α. Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen tailored immune response.

Lien vers HAL – hal-03451521

Lien vers le DOI – 10.1101/2021.01.19.427257