HCQ reverses aPL-mediated reduction of AnxA5 binding to phospholipid bilayers. (A) In the absence of HCQ, aPL IgGs (0.5 mg/mL) significantly reduced the binding of AnxA5 to PS/PC bilayers (quantity measured at 60 minutes: 0.10 ± 0.03 μg/cm² compared with 0.25 ± 0.01 μg/cm² for control IgG and β₂GPI; n = 3 pairs of different IgGs; P = .001). P values on graph denote differences between aPL and control IgGs (0.5 mg/mL). (B) In the presence of HCQ (1 mg/mL), binding of AnxA5 was restored to levels that were equivalent to control IgG (quantity measured at 60 minutes: 0.23 ± 0.03 μg/cm² vs 0.24 ± 0.03 μg/cm² for controls; P = .71). Interestingly, the presence of HCQ accelerated the binding of AnxA5 with control IgG, that is, even in the absence of aPL IgG.