{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T19:52:13Z","timestamp":1783021933091,"version":"3.54.6"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2025,3,6]],"date-time":"2025-03-06T00:00:00Z","timestamp":1741219200000},"content-version":"vor","delay-in-days":3017,"URL":"https:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Neutrophils act as a first line of defense against bacterial and fungal infections, but they are also important effectors of acute and chronic inflammation. Genome-wide association studies have established that the gene encoding the protein tyrosine phosphatase nonreceptor 22 (PTPN22) makes an important contribution to susceptibility to autoimmune disease, notably rheumatoid arthritis. Although PTPN22 is most highly expressed in neutrophils, its function in these cells remains poorly characterized. We show in this article that neutrophil effector functions, including adhesion, production of reactive oxygen species, and degranulation induced by immobilized immune complexes, were reduced in Ptpn22\u2212\/\u2212 neutrophils. Tyrosine phosphorylation of Lyn and Syk was altered in Ptpn22\u2212\/\u2212 neutrophils. On stimulation with immobilized immune complexes, Ptpn22\u2212\/\u2212 neutrophils manifested reduced activation of key signaling intermediates. Ptpn22\u2212\/\u2212 mice were protected from immune complex\u2013mediated arthritis, induced by the transfer of arthritogenic serum. In contrast, in vivo neutrophil recruitment following thioglycollate-induced peritonitis and in vitro chemotaxis were not affected by lack of PTPN22. Our data suggest an important role for PTPN22-dependent dephosphorylation events, which are required to enable full Fc\u03b3R-induced activation, pointing to an important role for this molecule in neutrophil function.<\/jats:p>","DOI":"10.4049\/jimmunol.1600604","type":"journal-article","created":{"date-parts":[[2016,11,3]],"date-time":"2016-11-03T02:03:34Z","timestamp":1478138614000},"page":"4771-4779","source":"Crossref","is-referenced-by-count":31,"title":["PTPN22 Is a Critical Regulator of Fc\u03b3 Receptor\u2013Mediated Neutrophil Activation"],"prefix":"10.1093","volume":"197","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8460-0884","authenticated-orcid":false,"given":"Sonja","family":"Vermeren","sequence":"first","affiliation":[{"name":"Medical Research Council\/University of Edinburgh Centre for Inflammation Research, Queen\u2019s Medical Research Institute , Edinburgh EH16 4TJ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine","family":"Miles","sequence":"additional","affiliation":[{"name":"Medical Research Council\/University of Edinburgh Centre for Inflammation Research, Queen\u2019s Medical Research Institute , Edinburgh EH16 4TJ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia Y","family":"Chu","sequence":"additional","affiliation":[{"name":"Medical Research Council\/University of Edinburgh Centre for Inflammation Research, Queen\u2019s Medical Research Institute , Edinburgh EH16 4TJ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4451-4375","authenticated-orcid":false,"given":"Donald","family":"Salter","sequence":"additional","affiliation":[{"name":"Institute for Genetics and Molecular Medicine , Edinburgh EH4 2XU,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9816-2638","authenticated-orcid":false,"given":"Rose","family":"Zamoyska","sequence":"additional","affiliation":[{"name":"Institute of Immunology and Infection Research, Ashworth Laboratories, University of Edinburgh , Edinburgh EH9 3FL,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7622-214X","authenticated-orcid":false,"given":"Mohini","family":"Gray","sequence":"additional","affiliation":[{"name":"Medical Research Council\/University of Edinburgh Centre for Inflammation Research, Queen\u2019s Medical Research Institute , Edinburgh EH16 4TJ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2016,12,15]]},"reference":[{"key":"2025030618360297900_r1","doi-asserted-by":"crossref","first-page":"266","DOI":"10.1046\/j.1365-2567.1997.00249.x","article-title":"Neutrophils from the synovial fluid of patients with rheumatoid arthritis express the high affinity immunoglobulin G receptor, Fc gamma RI (CD64): role of immune complexes and cytokines in induction of receptor expression","volume":"91","author":"Quayle","year":"1997","journal-title":"Immunology"},{"key":"2025030618360297900_r2","doi-asserted-by":"crossref","first-page":"515","DOI":"10.1136\/ard.53.8.515","article-title":"Role of Fc gamma receptors in the activation of neutrophils by soluble and insoluble immunoglobulin aggregates isolated from the synovial fluid of patients with rheumatoid arthritis","volume":"53","author":"Robinson","year":"1994","journal-title":"Ann. 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