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Platelet Activation Investigated in Pathogenesis of Lupus

Platelets activated by self-antigens may underlie disease by triggering interferon from immune cells

THURSDAY, Sept. 2 (HealthDay News) -- Platelet activation may play an important role in the pathogenesis of systemic lupus erythematosus (SLE), and it may present a target for therapy for the disease, according to research published in the Sept. 1 issue of Science Translational Medicine.

Pierre Duffau, of the Université Bordeaux in France, and colleagues discuss their focus on the CD154 protein -- also known as CD40 ligand -- which is found on T cells as well as the surface of activated platelets. They found that CD154 abundance and shedding from platelets in SLE patients was associated with disease severity.

In addition, when platelets from healthy individuals were exposed to serum from patients with active SLE or immune complexes like those found in patients, platelet activation and CD154 production were increased. The activated platelets then triggered production of interferon-α from antigen-presenting cells, continuing an inflammatory cycle. In mice with a propensity to develop lupus, depleting platelets or providing clopidogrel -- a P2Y(12) receptor antagonist -- improved survival and measures of disease, but transfusing activated platelets led to a worse disease course.

"Our results extend for human autoimmune disease the demonstration that activated platelets amplify the inflammatory response in a murine model of rheumatoid arthritis. Together, these observations open a possible therapeutic avenue for human inflammatory autoimmune diseases -- the long-term utilization of antiplatelet therapy," the authors conclude.

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