Figure 6
Figure 6. Role of IL-10 in complement-mediated IL-12 inhibition. (A) ELISA assays of plasma IL-10 levels in wild-type (WT) and DAF−/− mice 3 hours after LPS, CVF, or LPS/CVF treatment. (B) ELISA assays of plasma IL-12p40 levels in WT and IL-10−/− mice 3 hours after LPS or LPS/CVF treatment. (C) ELISA assays of IL-10 production by cultured WT mouse peritoneal macrophages 5 hours after LPS and/or C5a (50 nM) and C3a (200 nM) stimulation. (D) ELISA assays of IL-12p40 production by cultured WT mouse peritoneal macrophages 5 hours after LPS and/or C5a (50 nM) and C3a (200 nM) stimulation in the presence or absence of anti–IL-10 mAb (5 ng/mL). Four to 6 mice were used per group for panels A and B. Macrophages from 4 to 5 mice were pooled and assayed in triplicate in panels C and D. Values shown are the mean (± SEM). *P < .05, **P < .001, Student's t test.

Role of IL-10 in complement-mediated IL-12 inhibition. (A) ELISA assays of plasma IL-10 levels in wild-type (WT) and DAF−/− mice 3 hours after LPS, CVF, or LPS/CVF treatment. (B) ELISA assays of plasma IL-12p40 levels in WT and IL-10−/− mice 3 hours after LPS or LPS/CVF treatment. (C) ELISA assays of IL-10 production by cultured WT mouse peritoneal macrophages 5 hours after LPS and/or C5a (50 nM) and C3a (200 nM) stimulation. (D) ELISA assays of IL-12p40 production by cultured WT mouse peritoneal macrophages 5 hours after LPS and/or C5a (50 nM) and C3a (200 nM) stimulation in the presence or absence of anti–IL-10 mAb (5 ng/mL). Four to 6 mice were used per group for panels A and B. Macrophages from 4 to 5 mice were pooled and assayed in triplicate in panels C and D. Values shown are the mean (± SEM). *P < .05, **P < .001, Student's t test.

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