Figure 3.
Figure 3. Antibodies to β2GPI are responsible for thrombus formation in aPL-positive IgG-treated rats. The animals received LPS and 3 hours later aPL-positive IgG (□) or anti-β2GPI-depleted aPL-positive IgG (▪) from 3 patients with APS (A, C, and D). The number of thrombi (A) and vessel occlusions (B) were evaluated at various time intervals on 4 rats per group (1 sample, D, was repeated twice), and the results are expressed as mean ± SD. **P < .01 versus anti-β2GPI-depleted aPL-positive IgG. Immunofluorescence analysis of mesenteric tissue showing deposits of IgG in rats treated with aPL-positive IgG (C) or absence of IgG in rats receiving anti-β2GPI-depleted aPL-positive IgG (D). Original magnification, × 250. Details of image acquisition are given in Dobrina et al.23

Antibodies to β2GPI are responsible for thrombus formation in aPL-positive IgG-treated rats. The animals received LPS and 3 hours later aPL-positive IgG (□) or anti-β2GPI-depleted aPL-positive IgG (▪) from 3 patients with APS (A, C, and D). The number of thrombi (A) and vessel occlusions (B) were evaluated at various time intervals on 4 rats per group (1 sample, D, was repeated twice), and the results are expressed as mean ± SD. **P < .01 versus anti-β2GPI-depleted aPL-positive IgG. Immunofluorescence analysis of mesenteric tissue showing deposits of IgG in rats treated with aPL-positive IgG (C) or absence of IgG in rats receiving anti-β2GPI-depleted aPL-positive IgG (D). Original magnification, × 250. Details of image acquisition are given in Dobrina et al.23 

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