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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\n                    <jats:sup>\u2212<\/jats:sup>\n                    , PD-L1\n                    <jats:sup>lo<\/jats:sup>\n                    ] neutrophils produced inflammasome-dependent IL-1\u03b2 in the lungs in response to virulent mycobacteria and \u201caccelerated\u201d deleterious inflammation, which was highly exacerbated in IFN-\u03b3R\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Regulatory [MHC-II\n                    <jats:sup>+<\/jats:sup>\n                    , PD-L1\n                    <jats:sup>hi<\/jats:sup>\n                    ] neutrophils \u201cbrake\u201d inflammation by suppressing T-cell proliferation and IFN-\u03b3 production. Such beneficial regulation, which depends on PD-L1, is controlled by IFN-\u03b3R 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.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202402623","type":"journal-article","created":{"date-parts":[[2024,5,21]],"date-time":"2024-05-21T09:15:14Z","timestamp":1716282914000},"page":"e202402623","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":15,"title":["Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1\u03b2 or PD-L1"],"prefix":"10.26508","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3126-4004","authenticated-orcid":true,"given":"Emilie","family":"Doz-Deblauwe","sequence":"first","affiliation":[{"name":"INRAE, Universit\u00e9 de Tours, Nouzilly, 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