{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T07:14:14Z","timestamp":1790493254000,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2005,5,5]],"date-time":"2005-05-05T00:00:00Z","timestamp":1115251200000},"content-version":"vor","delay-in-days":4,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Lupus nephritis is characterized by immune complex deposition and inflammatory cell infiltration into the renal glomeruli. Local generation of chemokines and the presence of chemokine receptors on the infiltrating cells may be involved in this process. Fractalkine (Fkn)\/CX3CL1 and its receptor, CX3CR1, form one such chemokine system. We therefore undertook this study to investigate whether Fkn antagonist inhibits the initiation and progression of lupus nephritis in MRL\/<jats:italic>lpr<\/jats:italic> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>NH<jats:sub>2<\/jats:sub>\u2010terminally truncated Fkn\/CX3CL1 analogs were transfected into a nonmetastatic fibroblastoid cell line, MRL\/N\u20101, and injected subcutaneously into MRL\/<jats:italic>lpr<\/jats:italic> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Fkn analogs truncated by \u22654 amino acid residues from the N\u2010terminus failed to induce chemotaxis and calcium influx by CX3CR1\u2010expressing cells. Of these, the most potent antagonist (Fkn\u2010AT) lacked the 4 N\u2010terminal amino acid residues. Fkn expression in the glomerulus was significantly increased in 12\u2010week\u2010old MRL\/<jats:italic>lpr<\/jats:italic> mice. Expression was localized predominantly in the glomerular endothelial cells, but was occasionally observed in the mesangial cells and, to a lesser extent, in the interstitial microvasculature. Inoculation of MRL\/<jats:italic>lpr<\/jats:italic> mice with Fkn\u2010AT before the onset or during the early stages of lupus nephritis significantly reduced glomerular hypercellularity, glomerulosclerosis, crescent formation, and vasculitis compared with control mice. This seemed to be due to a marked reduction in macrophage accumulation. In contrast, Fkn antagonist did not affect pneumonitis, sialadenitis, lymphadenopathy, or splenomegaly.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>We prepared a novel potent Fkn antagonist and demonstrated its ability to delay the initiation and ameliorate the progression of lupus nephritis. This agent may therefore provide a new therapeutic approach to lupus nephritis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.21007","type":"journal-article","created":{"date-parts":[[2005,5,6]],"date-time":"2005-05-06T06:47:13Z","timestamp":1115362033000},"page":"1522-1533","source":"Crossref","is-referenced-by-count":110,"title":["Antagonist of fractalkine (CX3CL1) delays the initiation and ameliorates the progression of lupus nephritis in MRL\/<i>lpr<\/i> mice"],"prefix":"10.1002","volume":"52","author":[{"given":"Atsushi","family":"Inoue","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hitoshi","family":"Hasegawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masashi","family":"Kohno","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitsuko 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