{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T20:40:30Z","timestamp":1792010430362,"version":"4.4.0"},"reference-count":46,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2004,5,1]],"date-time":"2004-05-01T00:00:00Z","timestamp":1083369600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Lupus"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:p> Interleukin-6 (IL-6) is a pleiotropic cytokine with a wide range of biological activities that plays an important role in immune regulation and inflammation. Among other actions, it induces terminal differentiation of B lymphocytes into antibody-forming cells and the differentiation of T cells into effector cells. IL-6 also has multiple potent proinflammatory effects. An associationbetween IL-6 and lupus was demonstrated in murine models of SLE and blocking IL-6 improved lupus in all models tested. Data from several studies suggest that IL-6 plays a critical role in the B cell hyperactivity and immunopathology of human SLE, and may have a direct role in mediating tissue damage. Based on these data, we propose that blocking the effect of IL-6 in humans may improve lupus by interacting with the autoinflammatory process both systemically and locally. <\/jats:p>","DOI":"10.1191\/0961203304lu1023oa","type":"journal-article","created":{"date-parts":[[2004,5,26]],"date-time":"2004-05-26T22:54:21Z","timestamp":1085612061000},"page":"339-343","source":"Crossref","is-referenced-by-count":246,"title":["Rationale for interleukin-6 blockade in systemic lupus erythematosus"],"prefix":"10.1177","volume":"13","author":[{"given":"E","family":"Tackey","sequence":"first","affiliation":[{"name":"Office of the Clinical Director, National Institute of Arthritis and                         Musculoskeletal and Skin Diseases, National Institutes of Health, Department                         of Health and Human Services, Bethesda, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P E","family":"Lipsky","sequence":"additional","affiliation":[{"name":"Office of the Clinical Director, National Institute of Arthritis and                         Musculoskeletal and Skin Diseases, National Institutes of Health, Department                         of Health and Human Services, Bethesda, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G G","family":"Illei","sequence":"additional","affiliation":[{"name":"Office of the Clinical Director, National Institute of Arthritis and                         Musculoskeletal and Skin Diseases, National Institutes of Health, Department                         of Health and Human Services, Bethesda, 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