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. 2002 Nov;61(Suppl 2):ii46–ii50. doi: 10.1136/ard.61.suppl_2.ii46

Figure 4 .

Figure 4

C3 activation is required for aPL induced thrombophilia. (A) aPL-IgG induced thrombophilia is inhibited by Crry-Ig. CD-1 mice were injected ip with affinity purified aPL-IgG (aPL) or normal human (Cntrl IgG) at 0 hours and 48 hours. Half the mice in each group received Crry-Ig, and half the mice received control murine IgG (mIgG). At 72 hours after the first injection, surgically induced thrombus formation was measured as described in the text. There were 11–14 mice in each experimental group. Treatment with aPL-IgG caused an increase in thrombus size (*aPL + mIgG v Cntrl IgG + mIgG p<0.05), while Crry-Ig prevented aPL induced enhancement of thrombosis (*aPL + mIgG v aPL + Crry-Ig p<0.05; Cntrl IgG + Crry-Ig v aPL + Crry-Ig, p=NS). In a separate series of experiments, aPL did not significantly increase thrombosis in C3-/- mice (aPL v control IgG 1524 (825) µm v 1083 (443), p=NS). There was no difference in the levels of human aPL activity between C3+/+ mice and C3-/- mice. Reproduced from the J Exp Med 2001;195:217 by copyright permission of The Rockefeller Press.