{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:39:35Z","timestamp":1790775575447,"version":"4.1.0"},"reference-count":79,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2009,3,16]]},"abstract":"<jats:p>\u03b22 integrins and Fc\u03b3 receptors are critically involved in neutrophil activation at the site of inflammation. Both receptor types trigger a receptor-proximal tyrosine phosphorylation cascade through Src family kinases and Syk, but further downstream signaling events are poorly understood. We show that phospholipase C (PLC) \u03b32 is phosphorylated downstream of Src family kinases and Syk during integrin or Fc receptor-mediated activation of neutrophils. PLC\u03b32\u2212\/\u2212 neutrophils are completely defective in \u03b22 integrin or Fc\u03b3 receptor-mediated functional responses such as respiratory burst, degranulation, or cell spreading in vitro and show reduced adhesion\/spreading in inflamed capillary venules in vivo. However, PLC\u03b32\u2212\/\u2212 neutrophils respond normally to various other agonists, including chemokines, bacterial formyl peptides, Toll-like receptor ligands, or proinflammatory cytokines, and migrate normally both in vitro and in vivo. To confirm the in vivo relevance of these observations, the effect of the PLC\u03b32\u2212\/\u2212 mutation was tested in the K\/B\u00d7N serum transfer arthritis model, which is known to require \u03b22 integrins, Fc\u03b3 receptors, and neutrophils. PLC\u03b32 deficiency completely protected mice from clinical signs and histological features of arthritis as well as from arthritis-induced loss of articular function. These results identify PLC\u03b32 as a critical player of integrin and Fc receptor-mediated neutrophil functions and the neutrophil-mediated effector phase of autoimmune arthritis.<\/jats:p>","DOI":"10.1084\/jem.20081859","type":"journal-article","created":{"date-parts":[[2009,3,9]],"date-time":"2009-03-09T21:23:50Z","timestamp":1236633830000},"page":"577-593","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":114,"title":["Critical role of phospholipase C\u03b32 in integrin and Fc receptor-mediated neutrophil functions and the effector phase of autoimmune arthritis"],"prefix":"10.1084","volume":"206","author":[{"given":"Zolt\u00e1n","family":"Jakus","sequence":"first","affiliation":[{"name":"Department of Physiology, Semmelweis University School of Medicine, 1094 Budapest, Hungary 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edina","family":"Simon","sequence":"additional","affiliation":[{"name":"Department of Physiology, Semmelweis University School of Medicine, 1094 Budapest, Hungary 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Frommhold","sequence":"additional","affiliation":[{"name":"Department of Neonatology, University Children's Hospital, 69120 Heidelberg, Germany 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Sperandio","sequence":"additional","affiliation":[{"name":"Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians-University, 81377 Munich, Germany 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Attila","family":"M\u00f3csai","sequence":"additional","affiliation":[{"name":"Department of Physiology, Semmelweis University School of Medicine, 1094 Budapest, Hungary 1"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2009,3,9]]},"reference":[{"key":"2023072917142709200_bib1","doi-asserted-by":"crossref","first-page":"173","DOI":"10.1038\/nri1785","article-title":"Neutrophils and immunity: challenges and opportunities","volume":"6","author":"Nathan","year":"2006","journal-title":"Nat. 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