{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T20:22:40Z","timestamp":1789849360263,"version":"4.0.1"},"reference-count":42,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2008,5,31]],"date-time":"2008-05-31T00:00:00Z","timestamp":1212192000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Monosodium urate monohydrate (MSU) crystals are among the most potent proinflammatory stimuli, and an innate immune inflammatory response to the crystal surface is involved in the pathogenesis of gouty arthritis. Release of the crystals into the joint cavity promotes an acute inflammation characterized by massive infiltration of neutrophils, which leads to tissue damage. The aim of the present study was to assess the involvement of the tyrosine kinase Tec in MSU crystal\u2013initiated transduction events in human neutrophils.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Immunoprecipitation and immunoblotting techniques were used for the cellular signaling studies. Chemotaxis and enzyme\u2010linked immunosorbent assay techniques were used for the functional studies. Silencing of Tec expression using specific small interfering RNA was also performed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MSU crystals induced the phosphorylation and activation of Tec in a Src\u2010dependent manner. This activation was necessary for the MSU crystal\u2013induced secretion of interleukin\u20101\u03b2 (IL\u20101\u03b2) and IL\u20108 and for the generation of chemotactic activity in supernatants of MSU crystal\u2013stimulated neutrophils. In addition, colchicine, an effective drug for the treatment of gout, inhibited the MSU crystal\u2013induced tyrosine phosphorylation of Tec, thus modulating its kinase activity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings show that Tec is the principal kinase of the Tec family that plays a major role in the responses of human neutrophils to MSU crystals, which are likely to be involved in the initiation and perpetuation of gout. Our results suggest that the specific inhibition of Tec during the acute phase of MSU crystal\u2013induced inflammation may be considered for the treatment of gouty arthritis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.23801","type":"journal-article","created":{"date-parts":[[2008,5,31]],"date-time":"2008-05-31T21:46:41Z","timestamp":1212270401000},"page":"1866-1876","source":"Crossref","is-referenced-by-count":34,"title":["Crystal\u2010induced neutrophil activation: X. 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