ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection

Dan  Corral; Alison  Charton; Maria Eduarda Zancanaro Krauss; Eve  Blanquart; Florence  Levillain; Emma  Lefrançais; Tamara  Sneperger; Zoï  Vahlas; Jean-Philippe  Girard; Gérard Eberl; Yannick  Poquet; Jean-Charles  Guéry; Rafael J. Arguello; Yasmine Belkaid; Katrin D Mayer-Barber; Matthew Hepworth; Olivier  Neyrolles; Denis  Hudrisier

ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection

Dan Corral, Alison Charton, Maria Eduarda Zancanaro Krauss, Eve Blanquart, Florence Levillain, Emma Lefrançais, Tamara Sneperger, Zoï Vahlas, Jean-Philippe Girard, Gérard Eberl, Yannick Poquet, Jean-Charles Guéry, Rafael J. Arguello, Yasmine Belkaid, Katrin D Mayer-Barber, Matthew Hepworth, Olivier Neyrolles, Denis Hudrisier

Division of Immunology, Immunity to Infection and Respiratory Medicine

Research output: Contribution to journal › Article › peer-review

Abstract

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 lung IL-18R+ ILC toward a protective interferon--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 cell during secondary challenge with Mycobacterium tuberculosis (Mtb). Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen tailored immune response.

Original language	English
Journal	Cell Reports
Publication status	Accepted/In press - 29 Mar 2022

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Corral, D., Charton, A., Zancanaro Krauss, M. E., Blanquart, E., Levillain, F., Lefrançais, E., Sneperger, T., Vahlas, Z., Girard, J.-P., Eberl, G., Poquet, Y., Guéry, J.-C., Arguello, R. J., Belkaid, Y., Mayer-Barber, K. D., Hepworth, M., Neyrolles, O., & Hudrisier, D. (Accepted/In press). ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection. Cell Reports.

@article{7648900ec7ec4bdb84db5e612998f125,

title = "ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection",

abstract = "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 lung IL-18R+ ILC toward a protective interferon--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 cell during secondary challenge with Mycobacterium tuberculosis (Mtb). Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen tailored immune response.",

author = "Dan Corral and Alison Charton and {Zancanaro Krauss}, {Maria Eduarda} and Eve Blanquart and Florence Levillain and Emma Lefran{\c c}ais and Tamara Sneperger and Zo{\"i} Vahlas and Jean-Philippe Girard and G{\'e}rard Eberl and Yannick Poquet and Jean-Charles Gu{\'e}ry and Arguello, {Rafael J.} and Yasmine Belkaid and Mayer-Barber, {Katrin D} and Matthew Hepworth and Olivier Neyrolles and Denis Hudrisier",

year = "2022",

month = mar,

day = "29",

language = "English",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

}

Corral, D, Charton, A, Zancanaro Krauss, ME, Blanquart, E, Levillain, F, Lefrançais, E, Sneperger, T, Vahlas, Z, Girard, J-P, Eberl, G, Poquet, Y, Guéry, J-C, Arguello, RJ, Belkaid, Y, Mayer-Barber, KD, Hepworth, M, Neyrolles, O & Hudrisier, D 2022, 'ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection', Cell Reports.

TY - JOUR

T1 - ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection

AU - Corral, Dan

AU - Charton, Alison

AU - Zancanaro Krauss, Maria Eduarda

AU - Blanquart, Eve

AU - Levillain, Florence

AU - Lefrançais, Emma

AU - Sneperger, Tamara

AU - Vahlas, Zoï

AU - Girard, Jean-Philippe

AU - Eberl, Gérard

AU - Poquet, Yannick

AU - Guéry, Jean-Charles

AU - Arguello, Rafael J.

AU - Belkaid, Yasmine

AU - Mayer-Barber, Katrin D

AU - Hepworth, Matthew

AU - Neyrolles, Olivier

AU - Hudrisier, Denis

PY - 2022/3/29

Y1 - 2022/3/29

N2 - 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 lung IL-18R+ ILC toward a protective interferon--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 cell during secondary challenge with Mycobacterium tuberculosis (Mtb). Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen tailored immune response.

AB - 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 lung IL-18R+ ILC toward a protective interferon--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 cell during secondary challenge with Mycobacterium tuberculosis (Mtb). Collectively, our data reveal how tissue-resident ILCs adapt to type 1 inflammation toward a pathogen tailored immune response.

M3 - Article

SN - 2211-1247

JO - Cell Reports

JF - Cell Reports

ER -

ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection

Abstract

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