{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T21:03:07Z","timestamp":1791234187251,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,3,30]],"date-time":"2006-03-30T00:00:00Z","timestamp":1143676800000},"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":[[2006,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Mononuclear cell infiltration of the salivary glands is a major feature of Sj\u00f6gren's syndrome (SS) and its animal model. Local generation of chemokines and the presence of chemokine receptors on the infiltrating cells may be involved in this process. We undertook the present study to investigate the expression of chemokines during the development of autoimmune sialadenitis in MRL\/<jats:italic>lpr<\/jats:italic> mice and the therapeutic effect of chemokine antagonists on sialadenitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>NH<jats:sub>2<\/jats:sub>\u2010terminal\u2013truncated interferon\u2010inducible protein 10 (IP\u201010)\/CXCL10 analogs were transfected into a nonmetastatic fibroblastoid cell line, MRL\/N\u20101, and injected subcutaneously into MRL\/<jats:italic>lpr<\/jats:italic> mice, and the effects on sialadenitis were monitored.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>IP\u201010 analogs truncated by 5 or more amino acid residues from the N\u2010terminal failed to induce chemotaxis and calcium influx by CXCR3\u2010expressing cells. Of these, the most potent antagonist (AT) (IP\u201010\u2013AT) was a molecule with methionine added after removal of the 5 N\u2010terminal amino acid residues. Significantly increased expression of the Th1\u2010associated chemokines IP\u201010, monokine induced by interferon\u2010\u03b3\/CXCL9, and interferon\u2010inducible T cell chemoattractant\/CXCL11 was induced in the ductal epithelium by interferon\u2010\u03b3 produced in the salivary glands, whereas expression of the Th2\u2010associated chemokines thymus and activation\u2013regulated chemokine (TARC)\/CCL17 and monocyte\u2010derived chemokine\/CCL22 was almost undetectable during sialadenitis. Inoculation of IP\u201010\u2013AT into MRL\/<jats:italic>lpr<\/jats:italic> mice during the early stage of sialadenitis significantly reduced periductal mononuclear cell infiltration and parenchymal destruction compared with these features in control and TARC\u2010AT\u2013bearing mice. This was due to a significant reduction in infiltration of CXCR3+ T cells, predominantly Th1 cells, resulting in decreased interferon\u2010\u03b3 production.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>We prepared a novel potent IP\u201010 antagonist and demonstrated its ability to ameliorate the progression of autoimmune sialadenitis. This agent may provide a new therapeutic approach to SS.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.21745","type":"journal-article","created":{"date-parts":[[2006,3,30]],"date-time":"2006-03-30T18:16:52Z","timestamp":1143742612000},"page":"1174-1183","source":"Crossref","is-referenced-by-count":54,"title":["Antagonist of interferon\u2010inducible protein 10\/CXCL10 ameliorates the progression of autoimmune sialadenitis in MRL\/<i>lpr<\/i> 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