The monoclonal anti-PF4/polyanion antibody KKO preferentially binds to PF4 clusters, as formed in PF4/heparin complexes during heparin treatment (right panel, top) and on bacteria with high PF4-binding capacity (left panel, top). This can lead to heparin-induced thrombocytopenia (HIT) and to opsonization of bacteria. If the antibodies are present in high titer, they can promote formation of their own epitope by clustering PF4. This might be an explanation for delayed-onset HIT (right panel, bottom) and could augment opsonization of bacteria with low PF4 binding capacity.