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Here, we report pro-pathogenic crosstalk involving Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    granulocytes (Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra), IL-17, and COX2. We show that in the lungs of\n                    <jats:italic>Mtb<\/jats:italic>\n                    -infected wild-type mice, either BCG-vaccinated or not, most intracellular bacilli are Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra-resident 4 weeks post-infection onwards. In the genetically susceptible\n                    <jats:italic>\n                      ifng\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice, excessive Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra infiltration correlates with severe bacteremia. Neutralizing IL-17 (anti-IL17mAb) and COX2 inhibition by celecoxib reverse Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra infiltration, associated pathology, and death in\n                    <jats:italic>\n                      ifng\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice. Surprisingly, Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra also serves as the major source of IL-17 in the lungs of\n                    <jats:italic>Mtb<\/jats:italic>\n                    -infected WT or\n                    <jats:italic>\n                      ifng\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice. The IL-17-COX2-Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra interplay also operates in WT mice. Inhibiting ROR\u03b3t, the key transcription factor for IL-17 production or COX2, reduces the bacterial burden in Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra, leading to reduced bacterial burden and pathology in the lungs of WT mice. In the\n                    <jats:italic>Mtb<\/jats:italic>\n                    -infected WT mice, COX2 inhibition abrogates IL-17 levels in the lung homogenates and significantly enhances BCG\u2019s protective efficacy, mainly by targeting the Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra-resident\n                    <jats:italic>Mtb<\/jats:italic>\n                    pool, a phenotype also observed when IL-17 is blocked by ROR\u03b3t inhibitor. Furthermore, in pulmonary TB patients, high neutrophil count and IL-17 correlated with adverse treatment outcomes. Together, our results suggest that IL-17 and PGE2 are the negative correlates of protection, and we propose targeting the pro-pathogenic IL-17-COX2-Ly6G\n                    <jats:sup>+<\/jats:sup>\n                    Gra axis for TB prevention and therapy.\n                  <\/jats:p>","DOI":"10.7554\/elife.100966","type":"journal-article","created":{"date-parts":[[2024,9,25]],"date-time":"2024-09-25T17:14:01Z","timestamp":1727284441000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.100966","source":"Crossref","is-referenced-by-count":1,"title":["Ly6G+ granulocytes-derived IL-17 limits protective host responses and promotes tuberculosis pathogenesis"],"prefix":"10.7554","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-4553-1512","authenticated-orcid":true,"given":"Priya","family":"Sharma","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03j4rrt43","id-type":"ROR","asserted-by":"publisher"}],"name":"Cellular Immunology Group, International 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