Immune complex disintegration leads to good patient outcomes. Heparin-PF4 immune complex binds to FcγRIIA receptors on platelets. (A) HIT immune complex binding to platelets leads to thrombocytopenia and bleeding. (B) Cross-linking FcγRIIA receptors by platelet-bound immune complex leads to platelet activation, aggregation, granule/adenosine 5′-diphosphate (ADP) release, and thromboxane A2 synthesis. These and other prothrombotic processes (including neutrophil activation and NETosis) induce thrombosis, which results in adverse patient outcomes. (C) Immune complex dissociation by cationic UHRA inhibits A and B and results in good patient outcomes. Professional illustration by Somersault18:24.
