Immune thrombocytopenia (ITP) is a bleeding disorder rooted in abnormal B- and T-cell functions, causing platelet destruction. This is often triggered by antibodies targeting glycoprotein complexes on platelets, particularly GPIb/IX and GPIIb/IIIa. While phagocytosis by macrophages plays a role, recent studies suggest antibody-induced platelet changes, like desialylation and apoptosis, contribute to ITP. We examined 61 ITP patient sera, finding that antibodies led to significant platelet desialylation and apoptosis. Anti-GPIIb/IIIa antibodies increased neuraminidase 1 (NEU1) surface expression, while anti-GPIb/IX complex antibodies induced higher platelet apoptosis. In patients with anti-GPIIb/IIIa antibodies, FcγRIIa signaling drove desialylation and apoptosis, not platelet activation. Using an ITP mouse model, we found oseltamivir, a NEU1 inhibitor, prevented destruction by anti-GPIIb/IIIa antibodies. Further clinical trials exploring oseltamivir’s efficacy in treating ITP are warranted.
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