{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T07:29:01Z","timestamp":1765438141569},"reference-count":50,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2008,11,26]],"date-time":"2008-11-26T00:00:00Z","timestamp":1227657600000},"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":[[2008,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>The immunologic events that lead to persistent joint inflammation in certain patients with Lyme arthritis post\u2013antibiotic treatment have been elusive so far. The prevalence of this condition is highest in individuals with rheumatoid arthritis\u2013associated HLA\u2013DR alleles. This study was undertaken to generate a murine model with persistent arthritis post\u2013antibiotic treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We have previously shown that CD28<jats:sup>\u2212\/\u2212<\/jats:sup> mice develop intermittent monarticular Lyme arthritis that is responsive to antibiotics. Since there seems to be a link in humans between persistent arthritic manifestations post\u2013antibiotic treatment and the HLA\u2013DR4 allele, we generated DR4<jats:sup>+\/+<\/jats:sup>CD28<jats:sup>\u2212\/\u2212<\/jats:sup>MHCII<jats:sup>\u2212\/\u2212<\/jats:sup> mice, infected them with <jats:italic>Borrelia burgdorferi<\/jats:italic>, and subsequently treated them with antibiotics.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Thirty\u2010eight percent of the <jats:italic>B burgdorferi<\/jats:italic>\u2013infected DR4<jats:sup>+\/+<\/jats:sup>CD28<jats:sup>\u2212\/\u2212<\/jats:sup>MHCII<jats:sup>\u2212\/\u2212<\/jats:sup> mice, but none of the <jats:italic>B burgdorferi<\/jats:italic>\u2013infected CD28<jats:sup>\u2212\/\u2212<\/jats:sup>MHCII<jats:sup>\u2212\/\u2212<\/jats:sup> mice, remained arthritic post\u2013antibiotic treatment. A significant fraction (36%) of these mice, but none of the mice in which arthritis resolved, had serum antibodies to outer surface protein A of <jats:italic>B burgdorferi<\/jats:italic>. After abrogation of active <jats:italic>B burgdorferi<\/jats:italic> infection, the inflammatory reaction in mice with persistent joint inflammation was restricted to the joints, since their draining lymph nodes were no longer enlarged. Increased CD20 and interferon\u2010\u03b3 messenger RNA expression in the inflamed joints of these mice suggested a possible role of B cells and inflammatory cytokines in the pathogenesis of persistent arthritis post\u2013antibiotic treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The establishment of this murine model allows, for the first time, the elucidation of the immunologic events that lead to persistent Lyme arthritis post\u2013antibiotic therapy in genetically susceptible individuals.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.24028","type":"journal-article","created":{"date-parts":[[2008,11,29]],"date-time":"2008-11-29T11:46:59Z","timestamp":1227959219000},"page":"3892-3901","source":"Crossref","is-referenced-by-count":26,"title":["Persistent arthritis in <i>Borrelia burgdorferi\u2013<\/i>infected HLA\u2013DR4\u2013positive CD28\u2010negative mice post\u2013antibiotic treatment"],"prefix":"10.1002","volume":"58","author":[{"given":"Bettina 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