Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1 - INRAE - Institut national de recherche pour l’agriculture, l’alimentation et l’environnement Access content directly
Journal Articles Life Science Alliance Year : 2024

Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1

Badreddine Bounab
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Florence Carreras
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  • PersonId : 1206477
Mohamed Lamkanfi
Yves Le Vern
Pierre Germon
Julien Pichon
Florent Kempf
Aude Remot

Abstract

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-1β in the lungs in response to virulent mycobacteria and “accelerated” deleterious inflammation, which was highly exacerbated in IFN-γR −/− mice. Regulatory [MHC-II + , PD-L1 hi ] neutrophils “brake” inflammation by suppressing T-cell proliferation and IFN-γ production. Such beneficial regulation, which depends on PD-L1, is controlled by IFN-γR signaling in neutrophils. The hypervirulent HN878 strain from the Beijing genotype curbed PD-L1 expression by regulatory neutrophils, abolishing the braking function and driving deleterious hyperinflammation in the lungs. 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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hal-04596372 , version 1 (31-05-2024)

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Emilie Doz-Deblauwe, Badreddine Bounab, Florence Carreras, Julia S Fahel, Sergio C Oliveira, et al.. Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1. Life Science Alliance, 2024, 7 (7), pp.e202402623. ⟨10.26508/lsa.202402623⟩. ⟨hal-04596372⟩
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