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Here, we show that the myeloid Src-family kinases Hck, Fgr, and Lyn are critical for experimental models of gout, as well as for genetically determined systemic inflammation in the Ptpn6me-v\/me-v (motheaten viable) mouse model. The Hck\u2212\/\u2212Fgr\u2212\/\u2212Lyn\u2212\/\u2212 mutation abrogated various monosodium urate (MSU) crystal\u2013induced pro-inflammatory responses of neutrophils, and protected mice from the development of gouty arthritis. The Src-family inhibitor dasatinib abrogated MSU crystal\u2013induced responses of human neutrophils and reduced experimental gouty arthritis in mice. The Hck\u2212\/\u2212Fgr\u2212\/\u2212Lyn\u2212\/\u2212 mutation also abrogated spontaneous inflammation and prolonged the survival of the Ptpn6me-v\/me-v mice. Spontaneous adhesion and superoxide release of Ptpn6me-v\/me-v neutrophils were also abolished by the Hck\u2212\/\u2212Fgr\u2212\/\u2212Lyn\u2212\/\u2212 mutation. Excessive activation of tyrosine phosphorylation pathways in myeloid cells may characterize a subset of autoinflammatory diseases.<\/jats:p>","DOI":"10.1084\/jem.20221010","type":"journal-article","created":{"date-parts":[[2023,3,29]],"date-time":"2023-03-29T02:20:54Z","timestamp":1680056454000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Myeloid Src-family kinases are critical for neutrophil-mediated autoinflammation in gout and motheaten models"],"prefix":"10.1084","volume":"220","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1661-4635","authenticated-orcid":true,"given":"Krisztina","family":"Futosi","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01g9ty582","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Physiology, School of Medicine, Semmelweis University 1 , Budapest, 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