{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:35:30Z","timestamp":1787315730829,"version":"build-2736575974"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T00:00:00Z","timestamp":1498089600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,6,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Prolactin (PRL) is a neuroendocrine hormone that can promote inflammation. We examined the synovial tissue and fluid levels of PRL in patients with inflammatory arthritis, PRL expression in differentiated M\u03d5s from patients with arthritis and from healthy donors, and the effects of different stimuli on PRL production by M\u03d5s. PRL levels were measured in paired synovial fluid (SF) and peripheral blood of patients with rheumatoid arthritis (RA, n = 19), psoriatic arthritis (PsA, n = 11), and gout (n = 11). Synovial-tissue PRL mRNA expression was measured by quantitative PCR in patients with RA (n = 25), PsA (n = 11), and gout (n = 12) and in M\u03d5s differentiated in SF of patients with RA, PsA, other subtypes of spondyloarthritis (SpA), and gout. Synovial-tissue PRL mRNA expression correlated significantly with clinical disease parameters in patients with RA and PsA, including erythrocyte sedimentation rate (ESR, r = 0.424; P = 0.049) and disease activity score evaluated in 28 joints (DAS28, r = 0.729; P = 0.017). Synovial-tissue PRL expression was similar in RA, PsA, and gout. PRL mRNA expression was detected in monocyte-derived M\u03d5s from patients with RA and was significantly higher (P \u2264 0.01) in M\u03d5s differentiated in pooled SF from patients with RA and PsA compared with SpA or gout. PRL production by M\u03d5 differentiation in the SF from patients with RA was not further regulated by stimulation with CD40L, IgG, LPS, or TNF. PRL is produced locally in the synovium of patients with inflammatory arthritis. The production of PRL by M\u03d5s was increased by unknown components of RA and PsA SF, where it could contribute to disease progression.<\/jats:p>","DOI":"10.1189\/jlb.2a0317-115rr","type":"journal-article","created":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T20:40:18Z","timestamp":1498164018000},"page":"897-904","source":"Crossref","is-referenced-by-count":21,"title":["Rheumatoid arthritis and psoriatic arthritis synovial fluids stimulate prolactin production by macrophages"],"prefix":"10.1093","volume":"102","author":[{"given":"Man Wai","family":"Tang","sequence":"first","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"Department of Experimental Immunology, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel","family":"Garcia","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"Department of Experimental Immunology, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beatriz Malvar","family":"Fernandez","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"Department of Experimental Immunology, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle M","family":"Gerlag","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"GlaxoSmithKline , Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul-Peter","family":"Tak","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"GlaxoSmithKline , Stevenage, United Kingdom"},{"name":"Department of Rheumatology, Ghent University , Ghent, Belgium"},{"name":"Department of Rheumatology, University of Cambridge , Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kris A","family":"Reedquist","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"},{"name":"Department of Experimental Immunology, Academic Medical Center\/University of Amsterdam , Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,6,22]]},"reference":[{"key":"2023013012233040900_B1","doi-asserted-by":"crossref","first-page":"995","DOI":"10.1016\/S1567-5769(01)00045-5","article-title":"Estrogen, prolactin, and autoimmunity: actions and interactions","volume":"1","author":"McMurray","year":"2001","journal-title":"Int. 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