Anti–PECAM-1 MoAbs act as costimulatory agonists in ADP- and PAF-induced platelet aggregation. PRP was preincubated with (1) buffer, (2) normal mouse IgG₁, (3) PECAM-1.3, or (4) PECAM-1.2. All antibodies were used at a final concentration of 5 μg/mL. Note that PECAM-1.2 augmented low-dose (1.25 μmol/L) ADP-induced platelet aggregation, both in the absence (A) and presence (B) of the MoAb IV.3 (a blocking MoAb specific for FcγRIIa). The degree of potentiation of aggregation induced by PECAM-1.2 varied somewhat from experiment to experiment (compare [A] with [B]), and this variation was not attributable to FcγRIIa blockade. Incubation of PRP with increasing concentrations of PECAM-1.2 (shown in micrograms per milliliter), followed by the addition of either 2 μmol/L ADP (C) or 40 nmol/L PAF (D), showed that the effects of antibody-mediated dimerization of PECAM-1 are dose-dependent.