Only aPL antibodies that activate complement induce an increase in TF and fetal death in pregnant mice. (A) Pregnant mice were treated on days 8 and 12 of pregnancy with 2 different mouse monoclonal antibodies that recognize phospholipids on trophoblast cells. FB1 is an IgG2bκ that activates complement via classical pathway and FD1 is an IgG1κ that does not activate complement. A group of mice was treated with FB1 and the complement inhibitor Crry. On day 15, mice were killed and the frequency of fetal resorption was calculated (n = 6-7 mice/group). Mice that received FB1 had a high frequency of fetal resorption compared with those that received mIgG (P < .001). Administration of Crry protected mice from fetal death induced by FB1. Mice treated with FD1 did not show an increase in fetal resorption frequency that was observed with FB1. Error bars are SD. (B-D) Immunohistochemical analysis of decidual tissue from day 8 of pregnancy. Decidual tissue was processed for TF expression as described in “Materials and methods, Determination of TF functional activity in deciduas.” In FB1-treated mice (B), there was extensive TF deposition (brown) and embryo debris (ED). Treatment with Crry prevented the increase in TF expression in deciduas from FB1-treated mice (C). The decidual tissue from FD1-treated mice (D) showed minimal staining for TF in the ectoplacental cone (asterisk) and intact embryo comparable with mice treated with mIgG (not shown). Original magnification × 100.