Key result
Neutrophil, platelet, and interferon-α pathways drive systemic lupus erythematosus pathogenesis, supporting targeted combination therapies.
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The autoimmune disease systemic lupus erythematosus (SLE) results from an inability of the immune system to discriminate between certain self-antigens and foreign ones. The most common treatment of SLE involves the use of immunosuppressive drugs to reduce inflammation, but these therapies have serious side effects. Three recent papers in Science Translational Medicine redirect focus on neutrophils, platelets, and interferon-α in the pathogenesis of SLE and reinforce the notion that researchers should seek to discover and devise combination therapies that target these processes.
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Joseph Craft (2011) conducted an editorial in Systemic lupus erythematosus. Recent studies highlight the roles of neutrophils, platelets, and interferon-α in the pathogenesis of systemic lupus erythematosus, reinforcing the need for targeted combination therapies.
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