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Can Drug Effects Help Elucidate the Pathogenesis of SLE?

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Systemic lupus erythematosus (SLE) is a complex disease involving many different immune mechanisms, whose pathogenesis is not fully understood. In the past therapeutic interventions have employed medications with multiple immunological targets, making their use as probes of disease mechanisms difficult. For example, prednisone and cyclophosphamide, the most widely used therapies for severe disease until recently, affect such a broad array of immune mechanisms that they do not help identify the most important immunological SLE pathways. While examining the efficacy and toxicity of some of the new targeted therapies, this review will address what specific agents tell us about the pathogenesis of SLE. These include anti-CD20 and BlyS antibody, B and T cell co-stimulatory blockade such as anti- CD40L antibody and CTLA4Ig, therapies aimed at decreasing dsDNA specifically, as well as cytokine modulation with TNF alpha inhibitor, anti IL-10 ab, etc.





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Keywords: Systemic lupus erythematosus; pathogenesis; review; therapy

Document Type: Research Article

Affiliations: UCLA Medical School,Rheumatology Division, 1000 Veteran Avenue Rehabilitation Center, Room 32-59, Los Angeles, CA 98101, USA.

Publication date: 01 August 2006

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  • Current Rheumatology Reviews publishes frontier reviews on all the latest advances on rheumatology and its related areas e.g. pharmacology, pathogenesis, epidemiology, clinical care, and therapy. The journal's aim is to publish the highest quality review articles dedicated to clinical research in the field.

    The journal is essential reading for all researchers and clinicians in rheumatology.
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