{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T06:55:13Z","timestamp":1792652113327,"version":"4.5.0"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2010,3,26]],"date-time":"2010-03-26T00:00:00Z","timestamp":1269561600000},"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":[[2010,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Chemokines coordinate leukocyte trafficking in homeostasis and during immune responses. Prior studies of their role in arthritis have used animal models with both an initial adaptive immune response and an inflammatory effector phase. We undertook analysis of chemokines and their receptors in the effector phase of arthritis using the K\/BxN mouse serum\u2013transfer model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A time\u2010course microarray analysis of serum\u2010transferred arthritis was performed, examining ankle tissue, synovial fluid, and peripheral blood leukocytes. Up\u2010regulation of chemokines was confirmed by quantitative reverse transcriptase\u2013polymerase chain reaction. The functional relevance of chemokine induction was assessed by transferring serum into mice deficient in CCR1\u20137, CCR9, CXCR2, CXCR3, CXCR5, CX<jats:sub>3<\/jats:sub>CR1, CCL2, or CCL3. Further mechanistic analysis of CXCR2 involved treatment of arthritic mice with a CXCR2 antagonist, bone marrow (BM) cell transfers with CXCR2<jats:sup>+\/\u2212<\/jats:sup> and CXCR2<jats:sup>\u2212\/\u2212<\/jats:sup> donors and recipients, flow cytometry of synovial cells, and competition experiments measuring enrichment of CXCR2\u2010expressing neutrophils in arthritic joints of mice with mixed CXCR2<jats:sup>+\/+<\/jats:sup> and CXCR2<jats:sup>\u2212\/\u2212<\/jats:sup> BM cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Gene expression profiling revealed up\u2010regulation of the CXCR2 ligands CXCL1, CXCL2, and CXCL5 in the joint in parallel with disease activity. CXCR2<jats:sup>\u2212\/\u2212<\/jats:sup> mice had attenuated disease relative to CXCR2<jats:sup>+\/\u2212<\/jats:sup> littermates, as did mice receiving the CXCR2 inhibitor, while deficiency of other chemokine receptors did not affect arthritis severity. CXCR2 was required only on hematopoietic cells and was widely expressed on synovial neutrophils. CXCR2\u2010expressing neutrophils were preferentially recruited to arthritic joints in the presence of CXCR2\u2010deficient neutrophils.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>CXCR2 (but not other chemokine receptors) is critical for the development of autoantibody\u2010mediated arthritis, exhibiting a cell\u2010autonomous role in neutrophil recruitment to inflamed joints.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.27470","type":"journal-article","created":{"date-parts":[[2010,3,26]],"date-time":"2010-03-26T19:01:54Z","timestamp":1269630114000},"page":"1921-1932","source":"Crossref","is-referenced-by-count":101,"title":["Deficiency of CXCR2, but not other chemokine receptors, attenuates autoantibody\u2010mediated arthritis in a murine model"],"prefix":"10.1002","volume":"62","author":[{"given":"Jonathan 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