期刊
LUPUS
卷 14, 期 3, 页码 189-191出版社
SAGE PUBLICATIONS LTD
DOI: 10.1191/0961203305lu2134oa
关键词
infliximab; interferon-gamma; interleukins; nephritis; tumour necrosis factor
类别
In the course of the disease, a wide variety of cytokines is dysregulated, many of which likely influence systemic lupus erythematosus (SLE) autoimmunity and/or lupus tissue inflammation. Proinflammatory cytokines in particular, such as TNF, IL-6, IL-18 or IFN-gamma, may play a major role in propagating the inflammatory processes responsible for tissue damage. These cytokines are overexpressed both systemically and locally, and preliminary results from open-label trials and/or animal studies suggest potential benefits of blocking either of these inflammatory mediators. Since new therapeutic agents may soon offer many ways to influence the process, controlled clinical trials following open-label safety studies are of central importance to arrive at optimized therapies for SLE patients.
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