{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T11:37:24Z","timestamp":1790854644336,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2008,10,30]],"date-time":"2008-10-30T00:00:00Z","timestamp":1225324800000},"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":[[2008,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Human Lyme arthritis caused by <jats:italic>Borrelia burgdorferi<\/jats:italic> is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil\u2010activating protein A (NapA) of <jats:italic>B burgdorferi<\/jats:italic> in patients with Lyme arthritis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Serum anti\u2010NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Serum anti\u2010NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin\u201017 (IL\u201017) in response to NapA. Moreover, NapA was able to induce the expression of IL\u201023 in neutrophils and monocytes, as well as the expression of IL\u20106, IL\u20101\u03b2, and transforming growth factor \u03b2 (TGF\u03b2) in monocytes, via Toll\u2010like receptor 2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings indicate that NapA of <jats:italic>B burgdorferi<\/jats:italic> is able to drive the expression of IL\u20106, IL\u20101\u03b2, IL\u201023, and TGF\u03b2 by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.23972","type":"journal-article","created":{"date-parts":[[2008,10,30]],"date-time":"2008-10-30T11:04:01Z","timestamp":1225364641000},"page":"3609-3617","source":"Crossref","is-referenced-by-count":95,"title":["<i>Borrelia burgdorferi<\/i> NapA\u2013driven Th17 cell inflammation in lyme 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