Figure 1.
IC-FcγRIIA mediated platelet activation in human SLE. ICs induce platelet activation (A) and CD62P+ microvesicle release (B) in vitro (n = 5). (C) Quantification of serum ICs in patients with SLE (n = 73) and healthy volunteers (n = 30). (D) Quantification of CD41+CD62P+ circulating vesicles in the plasma of patients with SLE (n = 68) and healthy volunteers (n = 30). (E) Principal component (PC) analysis based on 3 variables: platelet activation, IC levels, and IgG+ platelets in patients with SLE and healthy volunteers. Correlation between the levels of activated platelets (αIIbβ3*+) with ICs (F) and with IgG+ platelets (G) in patients with SLE (n = 73). Data are presented as the mean ± SEM. Statistical analyses: 1-way analysis of variance (A-B), Wilcoxon test (C-D), and Spearman’s rank correlation (F-G). *P < .05, **P < .01. NS, nonstimulated.

IC-FcγRIIA mediated platelet activation in human SLE. ICs induce platelet activation (A) and CD62P+ microvesicle release (B) in vitro (n = 5). (C) Quantification of serum ICs in patients with SLE (n = 73) and healthy volunteers (n = 30). (D) Quantification of CD41+CD62P+ circulating vesicles in the plasma of patients with SLE (n = 68) and healthy volunteers (n = 30). (E) Principal component (PC) analysis based on 3 variables: platelet activation, IC levels, and IgG+ platelets in patients with SLE and healthy volunteers. Correlation between the levels of activated platelets (αIIbβ3*+) with ICs (F) and with IgG+ platelets (G) in patients with SLE (n = 73). Data are presented as the mean ± SEM. Statistical analyses: 1-way analysis of variance (A-B), Wilcoxon test (C-D), and Spearman’s rank correlation (F-G). *P < .05, **P < .01. NS, nonstimulated.

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