deg-anti-CD36 antibodies and deg-32-106 prevent FNAIT caused by maternal anti-CD36 antibodies. (A) Immunized Cd36^−/− female mice were bred with WT mice. During pregnancy, Cd36^−/− mothers were treated with deg-normal mouse IgG (cohort #6; n = 4), deg-anti-CD36 polyclonal antibodies (cohort #7; n = 3), or deg-32-106 (cohort #8; n = 6) in a dose of 5 mg/kg body weight on days 10, 15, and 20. The mortality of the pups treated with deg-anti-CD36 IgG (cohort #7; P < .01) or deg-32-106 (cohort #8; P < .0001) was significantly lower than that of mothers treated with deg-mouse IgG (cohort #6). Significance was analyzed by using the χ² test (**P < .01; ***P < .001). (B) WT mice platelets were incubated with mAb 32-106 (black) and deg-32-106 (green) using isotype IgG as controls (gray). The binding of both antibodies was compared by using flow cytometry. (C) As indicated, 50 ng deg-normal mouse IgG (red), 50 ng deg-32-106 (blue), or 5 ng deg-32-106 (green) was incubated with WT mice platelets. After washings, platelets were incubated with fluorescence-labeled (fluorescein isothiocyanate [FITC]) maternal IgG containing anti-CD36 antibodies (13.8 µg IgG) and analyzed by flow cytometry. Fluorescence-labeled (FITC) mouse IgG (dotted line) was used as a negative control. Note the significant left shift of fluorescence intensity in the presence of deg-32-106 compared with normal mouse IgG. (D) Alexa Fluor–labeled deg-32-106 (1 mg/kg) was injected into WT female mice via the tail vein. After 10 minutes, FITC-conjugated maternal IgG containing anti-CD36 antibodies was administered. Subsequently, the binding of anti-CD36 and deg-32-106 antibodies was evaluated at 30 and 60 minutes. Note the decreasing frequency of FITC-labeled platelets (Q2 + Q3) when deg-32-106 was injected (54.8% vs 34.9%; 35.5% vs 14.9%). A single administration of labeled deg-32-106 or maternal IgG containing anti-CD36 was run as a control.