{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T19:29:51Z","timestamp":1786562991491,"version":"build-2736575974"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,1,24]],"date-time":"2024-01-24T00:00:00Z","timestamp":1706054400000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82071752"],"award-info":[{"award-number":["82071752"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J of Rheum Dis"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>IL\u201038 is a recently discovered inflammatory factor that belongs to the IL\u20101 family and has full\u2010length and truncated forms. Clinical findings demonstrated that serum IL\u201038 levels in people with infectious and autoimmune diseases are significantly different from those in healthy people, but the form remains unclear. We are keenly interested in learning more about the regulatory role of full\u2010length IL\u201038 in rheumatoid arthritis (RA), a classic autoimmune disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>RA\u2010fibroblast\u2010like synoviocytes (RA\u2010FLS) were isolated from six RA patients and stimulated with full\u2010length IL\u201038 to observe IL\u20106 and IL\u20108 secretion. Then, the migration and invasion functions of FLS were assessed. Next, the protein expressions of the MAPK, NF\u2010\u03baB, and JAK pathways were evaluated. In addition, we examined the effect of full\u2010length IL\u201038 on FLS functions in the presence of IL\u20101\u03b2. The function of FLS affected by full\u2010length IL\u201038 was also examined after blocking IL\u20101 and IL\u201036 receptors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The functions of FLS were activated after the cells were stimulated with full\u2010length IL\u201038. IL\u20106 and IL\u20108 levels increased with an increase in the full\u2010length IL\u201038 concentration, and full\u2010length IL\u201038 induced the acceleration of FLS migration and invasion functions. In addition, the levels of proteins in the MAPK signaling pathway increased after stimulation with full\u2010length IL\u201038 and depended on its concentration. However, when the FLS were stimulated by IL\u201038 and IL\u20101\u03b2 simultaneously, all experiments generated opposite results. Full\u2010length IL\u201038 inhibited FLS function in the presence of IL\u20101\u03b2. IL\u20101R and IL\u201036R blockers terminated all effects of full\u2010length IL\u201038 on RA\u2010FLS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Full\u2010length IL\u201038 activates FLS functions and acts as a promoter in RA, whereas it inhibits FLS functions and acts as an inhibitor of RA in the presence of IL\u20101\u03b2. The function of full\u2010length IL\u201038 can be blocked by IL\u20101Ra and IL\u201036Ra.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1756-185x.15020","type":"journal-article","created":{"date-parts":[[2024,1,24]],"date-time":"2024-01-24T07:09:45Z","timestamp":1706080185000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Whether full\u2010length\n                    <scp>IL<\/scp>\n                    \u201038 acts as a promoter or inhibitor in activating rheumatoid arthritis fibroblast\u2010like synoviocytes depends on\n                    <scp>IL<\/scp>\n                    \u20101\u03b2"],"prefix":"10.1111","volume":"27","author":[{"given":"Yudan","family":"Ding","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology Zhujiang Hospital of Southern Medical University  Guangzhou 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