Dual neutrophil subsets accelerate or brake inflammation in tuberculosis - Emerg’in est une Infrastructure Nationale de Recherche pour la lutte contre les maladies infectieuses animales émergentes ou zoonotiques par l'exploration in vivo.
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Dual neutrophil subsets accelerate or brake inflammation in tuberculosis

Florence Carreras
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Yves Le Vern
Pierre Germon
Julien Pichon
Aude Remot
Nathalie Winter

Résumé

Neutrophils can be beneficial or deleterious during tuberculosis (TB). Based on the expression of MHC-II and programmed death ligand 1 (PD-L1), we distinguished two functionally and transcriptionally distinct neutrophil subsets in the lungs of mice infected with mycobacteria. Inflammatory [MHC-II-, PD-L1 lo ] neutrophils produced inflammasome-dependent IL-1b in the lungs in response to virulent mycobacteria and "accelerated" deleterious inflammation, which was highly exacerbated in IFN-gR -/-mice. Regulatory [MHC-II+, PD-L1 hi ] neutrophils "brake" inflammation by suppressing T-cell proliferation and IFN-g production. Such beneficial regulation, which depends on PD-L1, is controlled by IFN-gR signaling in neutrophils. These findings add a layer of complexity to the roles played by neutrophils in TB and may explain the reactivation of this disease observed in cancer patients treated with anti-PD-L1.

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Immunologie
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hal-04717343 , version 1 (01-10-2024)

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  • HAL Id : hal-04717343 , version 1

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Emilie Doz-Deblauwe, Badreddine Bounab, Florence Carreras, Julia Siveira Fahel, Sergio Oliveira, et al.. Dual neutrophil subsets accelerate or brake inflammation in tuberculosis. Neutrophil 2024, Sep 2024, Munich, Germany. . ⟨hal-04717343⟩
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