Figure 3
Figure 3. Detection of AVAs in IgG from patients with APS IgG. Levels of AVAs in the IgG of 27 patients with APS (19 VT and 8 PM) and 23 HC were analyzed by ELISA (A). IgG were tested in duplicates at 200 µg/mL, and binding was expressed in AUs in comparison with an in-house positive control. Dashed line depicts the cutoff for positivity, defined as values >3 SD above the mean in HCs (n = 23). Statistically significant difference (**P < .005, ***P < .001) was determined by ANOVA. The presence of AVA in patients with APS was correlated with VIM expression (protein fold change) on ex vivo healthy monocytes exposed to IgG derived from the same patients (B). Avidity of antibodies for VIM in a subset of APS-positive samples (C). Correlation between the induction of VIM (protein fold change) in monocytes by APS IgG and levels of AVAs (B) or high avidity antibodies (P = .0039) (D) is shown. 3D, 3-dimensional; AU, arbitrary unit; ELISA, enzyme-linked immunosorbent assay.

Detection of AVAs in IgG from patients with APS IgG. Levels of AVAs in the IgG of 27 patients with APS (19 VT and 8 PM) and 23 HC were analyzed by ELISA (A). IgG were tested in duplicates at 200 µg/mL, and binding was expressed in AUs in comparison with an in-house positive control. Dashed line depicts the cutoff for positivity, defined as values >3 SD above the mean in HCs (n = 23). Statistically significant difference (**P < .005, ***P < .001) was determined by ANOVA. The presence of AVA in patients with APS was correlated with VIM expression (protein fold change) on ex vivo healthy monocytes exposed to IgG derived from the same patients (B). Avidity of antibodies for VIM in a subset of APS-positive samples (C). Correlation between the induction of VIM (protein fold change) in monocytes by APS IgG and levels of AVAs (B) or high avidity antibodies (P = .0039) (D) is shown. 3D, 3-dimensional; AU, arbitrary unit; ELISA, enzyme-linked immunosorbent assay.

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