ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection.
Cell Rep
; 39(3): 110715, 2022 04 19.
Article
en En
| MEDLINE
| ID: mdl-35443177
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 (Mtb) infection alters the phenotype and function of lung IL-18Rα+ ILC toward a protective interferon-γ-producing ILC1-like population. This differentiation is controlled by type 1 cytokines and is associated with a glycolytic program. Moreover, a BCG-driven type I milieu enhances the early generation of ILC1-like cells during secondary challenge with Mtb. Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen-tailored immune response.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Tuberculosis
/
Inmunidad Innata
Límite:
Humans
Idioma:
En
Revista:
Cell Rep
Año:
2022
Tipo del documento:
Article