Platelet destruction by autoantibodies

This entry refers to the process by which autoantibodies target platelet membrane glycoproteins—most frequently glycoprotein IIb/IIIa and glycoprotein Ib-IX-V—leading to platelet destruction primarily in immune thrombocytopenia (ITP)[1][3][6][7]. Upon binding, these antibodies opsonize platelets, causing their sequestration and phagocytosis via Fc receptor-mediated mechanisms, predominantly in the spleen and liver. Additional mechanisms include complement activation, induction of platelet apoptosis, and desialylation, which further promote clearance[2][4][5]. This process is central to the pathophysiology of ITP and similar autoimmune disorders but is not itself a druggable molecule or receptor, rather representing an immunopathological pathway. Caveat: The designation "Platelet destruction by autoantibodies" is not a valid molecular target; it refers to a clinical phenomenon and underlying disease mechanism. For structured drug/target databases, entries should reference specific epitopes or molecules—such as "Platelet glycoprotein IIb/IIIa" or "Platelet glycoprotein Ib-IX"—rather than broad pathological processes.

Other names

Platelet antibody-mediated destructionImmune platelet clearanceAutoimmune platelet destructionITP-mediated platelet clearance

Fc receptor blockade (by IVIG); B cell depletion (by rituximab); Immunosuppression (by corticosteroids); Stimulation of platelet production (by TPO agonists)