Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the development of autoantibodies and immunologic attack of different organ systems, including the skin. This review aims to provide an overview of some of the pathogenic processes that may be important in the development of SLE, specifically cutaneous lupus erythematosus, and then illustrates how therapies might be tailored to modify these processes and treat disease.
Key points
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Cutaneous manifestations of lupus erythematosus occur frequently in systemic lupus erythematosus (SLE), may occur in the absence of systemic disease, and may precede the diagnosis of SLE.
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Proposed pathophysiologic mechanisms are common to cutaneous lupus erythematosus (CLE) and SLE, suggesting that response to skin disease may provide proof of principle for therapy for this disease.
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Ultraviolet (UV) light is a prominent trigger factor, and increased interferon (IFN)-α production is a common initiator of CLE.
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Novel treatment strategies are aimed at maximizing inhibition of IFN-α production and other potentially pathogenic cytokines.
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