{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T08:37:17Z","timestamp":1773477437568,"version":"3.50.1"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T00:00:00Z","timestamp":1740528000000},"content-version":"vor","delay-in-days":1944,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Alternatively activated macrophages are essential effector cells during type 2 immunity and tissue repair following helminth infections. We previously showed that Ym1, an alternative activation marker, can drive innate IL-1R\u2013dependent neutrophil recruitment during infection with the lung-migrating nematode, Nippostrongylus brasiliensis, suggesting a potential role for the inflammasome in the IL-1\u2013mediated innate response to infection. Although inflammasome proteins such as NLRP3 have important proinflammatory functions in macrophages, their role during type 2 responses and repair are less defined. We therefore infected Nlrp3\u2212\/\u2212 mice with N. brasiliensis. Unexpectedly, compared with wild-type (WT) mice, infected Nlrp3\u2212\/\u2212 mice had increased neutrophilia and eosinophilia, correlating with enhanced worm killing but at the expense of increased tissue damage and delayed lung repair. Transcriptional profiling showed that infected Nlrp3\u2212\/\u2212 mice exhibited elevated type 2 gene expression compared with WT mice. Notably, inflammasome activation was not evident early postinfection with N. brasiliensis, and in contrast to Nlrp3\u2212\/\u2212 mice, antihelminth responses were unaffected in caspase-1\/11\u2013deficient or WT mice treated with the NLRP3-specific inhibitor MCC950. Together these data suggest that NLRP3 has a role in constraining lung neutrophilia, helminth killing, and type 2 immune responses in an inflammasome-independent manner.<\/jats:p>","DOI":"10.4049\/jimmunol.1900640","type":"journal-article","created":{"date-parts":[[2019,10,4]],"date-time":"2019-10-04T17:04:41Z","timestamp":1570208681000},"page":"2724-2734","source":"Crossref","is-referenced-by-count":25,"title":["Inflammasome-Independent Role for NLRP3 in Controlling Innate Antihelminth Immunity and Tissue Repair in the Lung"],"prefix":"10.1093","volume":"203","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8755-461X","authenticated-orcid":false,"given":"Alistair L","family":"Chenery","sequence":"first","affiliation":[{"name":"Wellcome Centre for Cell-Matrix Research , Manchester M13 9PT ,","place":["United Kingdom"]},{"name":"Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester , Manchester M13 9PL ,","place":["United 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