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

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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<sup>-</sup>, PD-L1<sup>lo</sup>] 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<sup>-/-</sup> mice. Regulatory [MHC-II<sup>+</sup>, PD-L1<sup>hi</sup>] 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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MLA
Doz-Deblauwe, Emilie, et al. “Dual Neutrophil Subsets Exacerbate or Suppress Inflammation in Tuberculosis via IL-1β or PD-L1.” LIFE SCIENCE ALLIANCE, vol. 7, no. 7, 2024, doi:10.26508/lsa.202402623.
APA
Doz-Deblauwe, E., Bounab, B., Carreras, F., Fahel, J. S., Oliveira, S. C., Lamkanfi, M., … Winter, N. (2024). Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1. LIFE SCIENCE ALLIANCE, 7(7). https://doi.org/10.26508/lsa.202402623
Chicago author-date
Doz-Deblauwe, Emilie, Badreddine Bounab, Florence Carreras, Julia S Fahel, Sergio C Oliveira, Mohamed Lamkanfi, Yves Le Vern, et al. 2024. “Dual Neutrophil Subsets Exacerbate or Suppress Inflammation in Tuberculosis via IL-1β or PD-L1.” LIFE SCIENCE ALLIANCE 7 (7). https://doi.org/10.26508/lsa.202402623.
Chicago author-date (all authors)
Doz-Deblauwe, Emilie, Badreddine Bounab, Florence Carreras, Julia S Fahel, Sergio C Oliveira, Mohamed Lamkanfi, Yves Le Vern, Pierre Germon, Julien Pichon, Florent Kempf, Christophe Paget, Aude Remot, and Nathalie Winter. 2024. “Dual Neutrophil Subsets Exacerbate or Suppress Inflammation in Tuberculosis via IL-1β or PD-L1.” LIFE SCIENCE ALLIANCE 7 (7). doi:10.26508/lsa.202402623.
Vancouver
1.
Doz-Deblauwe E, Bounab B, Carreras F, Fahel JS, Oliveira SC, Lamkanfi M, et al. Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1. LIFE SCIENCE ALLIANCE. 2024;7(7).
IEEE
[1]
E. Doz-Deblauwe et al., “Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1,” LIFE SCIENCE ALLIANCE, vol. 7, no. 7, 2024.
@article{01J03JZ89T2SFM5AEQ8665G20Z,
  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<sup>-</sup>, PD-L1<sup>lo</sup>] 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<sup>-/-</sup> mice. Regulatory [MHC-II<sup>+</sup>, PD-L1<sup>hi</sup>] 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.}},
  articleno    = {{e202402623}},
  author       = {{Doz-Deblauwe, Emilie and Bounab, Badreddine and Carreras, Florence and Fahel, Julia S and Oliveira, Sergio C and Lamkanfi, Mohamed and Le Vern, Yves and Germon, Pierre and Pichon, Julien and Kempf, Florent and Paget, Christophe and Remot, Aude and Winter, Nathalie}},
  issn         = {{2575-1077}},
  journal      = {{LIFE SCIENCE ALLIANCE}},
  language     = {{eng}},
  number       = {{7}},
  pages        = {{16}},
  title        = {{Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1}},
  url          = {{http://doi.org/10.26508/lsa.202402623}},
  volume       = {{7}},
  year         = {{2024}},
}

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