{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T12:09:19Z","timestamp":1790856559001,"version":"4.1.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2009,11,1]],"date-time":"2009-11-01T00:00:00Z","timestamp":1257033600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The cyclooxygenase (COX) enzymes are known modulators of innate immune cell function; however, their contributions to adaptive immunity are relatively unknown. We investigated the roles of COX-1 and COX-2 in the humoral immune response to infection with the Lyme disease pathogen Borrelia burgdorferi. We report that in vitro, murine B cells constitutively expressed COX-1 and up-regulated expression of both COX-1 and COX-2 as well as their products PGE2, PGF2\u03b1, and thromboxane B2 and their receptors following stimulation with B. burgdorferi or anti-CD40. In vitro inhibition of COX-1 and\/or COX-2 in murine B cells resulted in decreased eicosanoid production and altered Ab production. Importantly, infection of mice lacking COX-1, but not COX-2, activity resulted in a defect in Ig class-switching and a lack of Borrelia-specific IgG production. This defect correlated with decreased germinal center formation and IL-6 and IL-17 production, and it could be partially recovered by restoration of IL-6, but fully recovered by IL-17. Furthermore, sera from COX-1 inhibitor-treated mice were dramatically less effective in killing B. burgdorferi, but borreliacidal activity was restored in COX-1 inhibitor-treated mice administered IL-17. We conclude that IL-17 plays a role in Ab production and Ig class-switching in response to infection and that COX-1 is a critical, previously unrecognized regulator of this response.<\/jats:p>","DOI":"10.4049\/jimmunol.0901499","type":"journal-article","created":{"date-parts":[[2009,10,20]],"date-time":"2009-10-20T17:42:08Z","timestamp":1256060528000},"page":"5644-5653","source":"Crossref","is-referenced-by-count":38,"title":["Cyclooxygenase-1 Orchestrates Germinal Center Formation and Antibody Class-Switch via Regulation of IL-17"],"prefix":"10.1093","volume":"183","author":[{"given":"Victoria A","family":"Blaho","sequence":"first","affiliation":[{"name":"Department of Veterinary Pathobiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew W","family":"Buczynski","sequence":"additional","affiliation":[{"name":"Department of Pharmacology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward A","family":"Dennis","sequence":"additional","affiliation":[{"name":"Department of Pharmacology"},{"name":"Department of Chemistry and Biochemistry, University of California , San Diego, La Jolla, CA 92093"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R","family":"Brown","sequence":"additional","affiliation":[{"name":"Department of Veterinary Pathobiology"},{"name":"Department of Molecular Microbiology and Immunology, University of Missouri , Columbia, MO 65211"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,11,1]]},"reference":[{"key":"2026012811141764700_R1","first-page":"73","article-title":"Cytokines and chemokines shaping the B-cell compartment.","volume-title":"Cytokine Growth Factor Rev.","year":"2007"},{"key":"2026012811141764700_R2","first-page":"1895","article-title":"Interleukin-6 influences germinal center development and antibody production via a contribution of C3 complement component.","volume-title":"J. 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