Prothrombotic Platelets: A New Channel for Inflammation in Antiphospholipid Syndrome
A new study in Arthritis & Rheumatology reveals a key mechanism driving thrombosis in antiphospholipid syndrome (APS), an autoimmune disorder characterized by abnormal blood clots. Researchers found that platelets from APS patients exhibit significantly higher basal release of ATP, a key inflammatory signaling molecule. This release occurs primarily through pannexin-1 (PANX1) channels, which are abnormally activated. The study demonstrated that antibodies from APS patients trigger phosphorylation of PANX1, leading to excessive ATP release, which in turn activates P2X receptors and calcium-dependent signaling cascades that amplify platelet activation, P-selectin exposure, and aggregation. Inhibiting PANX1 with carbenoxolone normalized ATP release and reduced prothrombotic platelet responses, identifying this channel as a novel therapeutic target.
Why it might matter to you:
This research directly connects innate immune signaling—specifically, antibody-mediated activation of a purinergic channel—to a hypercoagulable state. For immunologists focused on humoral immunity and inflammation, it illustrates how autoantibodies can dysregulate fundamental cellular physiology beyond simple opsonization or complement activation. The identification of PANX1 as a central player offers a precise target for immunotherapy that could inhibit pathological thrombosis without compromising essential hemostasis, a significant advance over broader anticoagulant strategies.
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