Cooperative effect between anti-PF4/H and anti-PF4 antibodies increases cell activation and thrombotic risk in HIT.

ABSTRACT:

Abstract

Heparin-induced thrombocytopenia (HIT) is a severe complication of heparin therapy, frequently associated with thrombosis. Immunoglobulin G (IgG) antibodies to heparin-platelet factor 4 (PF4/H) complexes play a central role in HIT by activating platelets and leukocytes via Fc gamma Receptor IIa (FcγRIIA). However, some patients also develop IgG against unmodified PF4 (anti-PF4), but their implication in the pathophysiology of HIT is unclear. Therefore, we assessed the impact of the joint presence of anti-PF4/H and anti-PF4 antibodies on cellular activation, platelet count, and thrombus formation, using chimeric monoclonal IgG1 antibodies specific for either PF4/H complexes (5B9) or PF4 alone (1E12). As expected, 5B9 coincubated with washed platelets without heparin did not

SUBMITTER: Billy S 

PROVIDER: S-EPMC12432984 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature