{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:01:06Z","timestamp":1791198066130,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2011,8,1]],"date-time":"2011-08-01T00:00:00Z","timestamp":1312156800000},"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":[[2011,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To examine whether synovial interleukin\u201017 (IL\u201017) expression promotes tumor necrosis factor (TNF)\u2013induced joint pathologic processes in vivo, and to analyze the surplus ameliorative value of neutralizing IL\u201017 in addition to TNF during collagen\u2010induced arthritis (CIA).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Adenoviral vectors were used to induce overexpression of IL\u201017 and\/or TNF in murine knee joints. In addition, mice with CIA were treated, at different stages of arthritis, with soluble IL\u201017 receptor (sIL\u201017R), TNF binding protein (TNFBP), or the combination.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Overexpression of IL\u201017 and TNF resulted in joint inflammation and bone erosion in murine knees. Interestingly, IL\u201017 strikingly enhanced both the joint\u2010inflammatory and joint\u2010destructive capacity of TNF. Further analysis revealed a strongly enhanced up\u2010regulation of S100A8, IL\u20101\u03b2, and matrix metalloproteinase (MMP) messenger RNA, only when both TNF and IL\u201017 were present. Moreover, the increase in irreversible cartilage destruction was not merely the result of enhanced inflammation, but also was associated with a direct synergistic effect of these cytokines in the joint. S100A9 deficiency in mice protected against IL\u201017\/TNF\u2013induced expression of cartilage NITEGE neoepitopes. During established arthritis, the combination of sIL\u201017R and TNFBP was more effective than the anticytokine treatments alone, and significantly inhibited further joint inflammation and cartilage destruction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Local synovial IL\u201017 expression enhances the role of TNF in joint destruction. Synergy between TNF and IL\u201017 in vivo results in striking exaggeration of cartilage erosion, in parallel with a synergistic up\u2010regulation of S100A8, IL\u20101\u03b2, and erosive MMPs. Moreover, neutralizing IL\u201017 in addition to TNF further improves protection against joint damage and is still effective during late\u2010stage CIA. Therefore, compared with anti\u2010TNF alone, combination blocking of TNF and IL\u201017 may have additional therapeutic value for the treatment of destructive arthritis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.30418","type":"journal-article","created":{"date-parts":[[2011,4,22]],"date-time":"2011-04-22T14:34:44Z","timestamp":1303482884000},"page":"2329-2339","source":"Crossref","is-referenced-by-count":125,"title":["Tumor necrosis factor\u2013interleukin\u201017 interplay induces S100A8, interleukin\u20101\u03b2, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis"],"prefix":"10.1002","volume":"63","author":[{"given":"Marije I.","family":"Koenders","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renoud J.","family":"Marijnissen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabel","family":"Devesa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Lubberts","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leo A. 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