American Society of Hematology

Figure 4.

$Figure 4. Cardiolipin reactivity of polyclonal aPLs is required and sufficient for rapid TF activation. (A) Human MM1 cells were stimulated in the presence or absence of C3 inhibitor compstatin (50 µM) or PDI inhibitor 16F16 (2 µM) for 15 minutes at 37°C with IgG fractions isolated from 20 APS patients or 20 healthy controls. APS patient IgG samples can be divided into 3 groups: patient IgG that bind only to cardiolipin (CL) in a cofactor-independent manner similar to HL5B (CL; n = 11); patient IgG that bind to both antigens similar to HL7G (CL + β2GPI; n = 7); and patient IgG that bind only to β2GPI similar to rJGG9 (β2GPI; n = 2). Cell-associated PCA was subsequently measured by single-stage clotting assay; *P < .0001; 1-way ANOVA followed by the Dunnett multiple-comparison test. (B) MM1 cells were stimulated for 10 minutes with IgG fractions as described in panel A and PS exposure was quantified with Annexin V–FITC by flow cytometry.$

Cardiolipin reactivity of polyclonal aPLs is required and sufficient for rapid TF activation. (A) Human MM1 cells were stimulated in the presence or absence of C3 inhibitor compstatin (50 µM) or PDI inhibitor 16F16 (2 µM) for 15 minutes at 37°C with IgG fractions isolated from 20 APS patients or 20 healthy controls. APS patient IgG samples can be divided into 3 groups: patient IgG that bind only to cardiolipin (CL) in a cofactor-independent manner similar to HL5B (CL; n = 11); patient IgG that bind to both antigens similar to HL7G (CL + β2GPI; n = 7); and patient IgG that bind only to β2GPI similar to rJGG9 (β2GPI; n = 2). Cell-associated PCA was subsequently measured by single-stage clotting assay; *P < .0001; 1-way ANOVA followed by the Dunnett multiple-comparison test. (B) MM1 cells were stimulated for 10 minutes with IgG fractions as described in panel A and PS exposure was quantified with Annexin V–FITC by flow cytometry.

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