{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T03:01:14Z","timestamp":1788490874857,"version":"build-2803163510"},"reference-count":170,"publisher":"Wiley","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Biomedicine and Biotechnology"],"published-print":{"date-parts":[[2012]]},"abstract":"<jats:p>\n                    SLE is an autoimmune inflammatory disease in which various pro- and anti-inflammatory cytokines, including TGF-\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , IL-10, BAFF, IL-6, IFN-\n                    <jats:italic>\u03b1<\/jats:italic>\n                    , IFN-\n                    <jats:italic>\u03b3<\/jats:italic>\n                    , IL-17, and IL-23, play crucial pathogenic roles. Virtually, all these cytokines can be generated by both innate and adaptive immune cells and exert different effects depending on specific local microenvironment. They can also interact with each other, forming a complex network to maintain delicate immune homeostasis. 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