Figure 6. Dectin-2 is required for CAWS-induced CCL2 production and the development of vasculitis.

(A) F4/80⁺ cells isolated from the heart were stimulated with CAWS (10 μg/mL) for 18 hours and CCL2 protein in the culture supernatant was measured by ELISA (mean ± SEM from 2 experiments; *P = 0.001 versus unstimulated). (B) Wild-type and Dectin-2^–/– mice were injected with CAWS, and 1 day later hearts were harvested and assessed for Ccl2 mRNA expression by qPCR (mean ± SEM, n = 4–6 from 2 experiments, *P < 0.0001 versus WT). (C) Vasculitis scores of Tlr4^–/–, Tlr2^–/–, Dectin-1^–/–, or Dectin-2^–/– mice on day 28 after CAWS injection (mean ± SEM, n = 4–8 mice per group, *P < 0.001 versus WT). (D) H&E–stained aortic root lesions isolated from Tlr4^–/–, Tlr2^–/–, Dectin-1^–/–, or Dectin-2^–/– mice on day 28. Scale bars: 400 μm. (E) Vasculitis scores of FcγR^–/– or Card9^–/– mice on day 28 after CAWS injection (mean ± SEM, *P < 0.0001 versus WT). (F) Vasculitis scores of CD11cΔSyk mice or control mice (Syk^fl/fl) on day 28 after CAWS injection (mean ± SEM, *P < 0.0001 versus Syk^fl/fl). (G) CD11cΔSyk mice or control mice were injected with CAWS, and 1 day later, heart tissues were harvested and assessed for Ccl2 RNA expression by qPCR (mean ± SEM, n = 4 mice per group, *P < 0.001 versus Syk^fl/fl). P values were calculated using unpaired 2-tailed Student’s t test (A, B, F, and G) or 1-way ANOVA with Dunnett’s post hoc test (C and E).