{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T00:31:53Z","timestamp":1768005113736,"version":"3.49.0"},"reference-count":22,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,9,26]],"date-time":"2016-09-26T00:00:00Z","timestamp":1474848000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004885","name":"Ume\u00e5 Universitet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004885","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100008267","name":"Kong Christian den Tiendes Fond","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100008267","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100008249","name":"Frimodt-Heineke Fonden","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100008249","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2016,10]]},"abstract":"Abstract<\/jats:title>Rheumatoid arthritis (RA<\/jats:styled-content>) is caused by complex interactions between immune cells and sustained by Th1 response cytokines. Resistin [resistance to insulin; (RETN)<\/jats:styled-content>] is an inflammatory cytokine, first discovered in murine adipocytes. In man, RETN<\/jats:styled-content> is mainly secreted by monocytes. The distinct role of RETN<\/jats:styled-content> in the immune reaction is uncertain; however, RETN<\/jats:styled-content> has pro\u2010inflammatory, pro\u2010fibrotic and possibly tolerogenic properties. The aim was to assess the reaction of RETN<\/jats:styled-content> gene expression to TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic> inhibition (I) in pathogenetic immune cell subsets in RA<\/jats:styled-content>, in the context of Th1, inflammatory and regulatory cytokine gene expressions. Accordingly, we measured RETN<\/jats:styled-content>, IFN<\/jats:styled-content>\u2010\u03b3<\/jats:italic>, TNF<\/jats:styled-content>\u2010\u03b2<\/jats:italic>, IL<\/jats:styled-content>\u20101\u03b2<\/jats:italic>, TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic>, TGF<\/jats:styled-content>\u2010\u03b2<\/jats:italic> and IL<\/jats:styled-content>\u201010 gene expressions in CD<\/jats:styled-content>14+<\/jats:sup> monocytes, CD<\/jats:styled-content>4+<\/jats:sup> T helper (Th) lymphocytes (ly), CD<\/jats:styled-content>8+<\/jats:sup> T cytotoxic (Tc) ly and CD<\/jats:styled-content>19+<\/jats:sup> B ly in active RA<\/jats:styled-content> before and 3\u00a0months after start of TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic>I. Leucocyte subsets were separated by specific monoclonal antibody\u2010covered beads, RNA<\/jats:styled-content> extracted and levels of RETN<\/jats:styled-content>, Th1 response, inflammatory and regulatory cytokine mRNA<\/jats:styled-content>s measured by quantitative reverse transcription\u2010polymerase chain reaction technique. We found that TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic>I caused a significant downregulation of RETN<\/jats:styled-content> gene expression in CD<\/jats:styled-content>14+<\/jats:sup> monocytes and CD<\/jats:styled-content>4+<\/jats:sup> Th ly and was unchanged in CD<\/jats:styled-content>8+<\/jats:sup> Tc ly and CD<\/jats:styled-content>19+<\/jats:sup> B ly. Both in active RA<\/jats:styled-content> and during TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic>I, RETN mRNA<\/jats:styled-content> levels were significantly higher in CD<\/jats:styled-content>14+<\/jats:sup> monocytes than in all other examined cell types. In monocytes, fold change in RETN<\/jats:styled-content> and TGF<\/jats:styled-content>\u2010\u03b2<\/jats:italic> gene expressions upon TNF<\/jats:styled-content>\u2010\u03b1<\/jats:italic>I correlated significantly. Our findings indicate that RETN<\/jats:styled-content> has pro\u2010inflammatory as well as proresolving roles in active RA.<\/jats:p>","DOI":"10.1111\/sji.12464","type":"journal-article","created":{"date-parts":[[2016,7,19]],"date-time":"2016-07-19T14:52:57Z","timestamp":1468939977000},"page":"229-236","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Resistin Gene Expression is Downregulated in CD<\/scp>4+<\/sup> T\u00a0Helper Lymphocytes and CD<\/scp>14+<\/sup> Monocytes in Rheumatoid Arthritis Responding to TNF<\/scp>\u2010\u03b1<\/i> Inhibition"],"prefix":"10.1111","volume":"84","author":[{"given":"I.","family":"Nagaev","sequence":"first","affiliation":[{"name":"Division of Clinical Immunology Department of Clinical Microbiology Norrland's University Hospital Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Andersen","sequence":"additional","affiliation":[{"name":"Department of Medicine North Denmark Regional Hospital\/Department of Health Science and Technolgy University of Aalborg Aalborg Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. K.","family":"Olesen","sequence":"additional","affiliation":[{"name":"Department of Medicine North Denmark Regional Hospital\/Department of Health Science and Technolgy University of Aalborg Aalborg Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"O.","family":"Nagaeva","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology Department of Clinical Microbiology Norrland's University Hospital Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Wikberg","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Biosciences Uppsala University Uppsala Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Mincheva\u2010Nilsson","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology Department of Clinical Microbiology Norrland's University Hospital Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. N.","family":"Andersen","sequence":"additional","affiliation":[{"name":"Department of Rheumatology North Denmark Regional Hospital\/Department of Clinical Medicine Aalborg University Aalborg Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2016,9,26]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/35053000"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2003.07.003"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0010045"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.5173"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.50.10.2199"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0000031"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvs.2011.10.011"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.4067\/S0716-97602013000100002"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1004579"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2011.04.006"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2172-11-33"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2006.054734"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.9.5789"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.27473"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-0031-1287783"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00394-013-0599-2"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.27584"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2008.112797"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.258731"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0041373"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.24568"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2010.143768"}],"container-title":["Scandinavian Journal of Immunology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1111%2Fsji.12464","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/sji.12464","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,9,29]],"date-time":"2023-09-29T19:25:31Z","timestamp":1696015531000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/sji.12464"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016,9,26]]},"references-count":22,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2016,10]]}},"alternative-id":["10.1111\/sji.12464"],"URL":"https:\/\/doi.org\/10.1111\/sji.12464","archive":["Portico"],"relation":{},"ISSN":["0300-9475","1365-3083"],"issn-type":[{"value":"0300-9475","type":"print"},{"value":"1365-3083","type":"electronic"}],"subject":[],"published":{"date-parts":[[2016,9,26]]},"assertion":[{"value":"2016-07-11","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2016-07-16","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2016-09-26","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}