IL-4 enhances efferocytosis of X-CGD RPMØs via 12/15-LO–dependent PPARγ activation. (A) RPMØs were treated either with IL-4, rosiglitazone, GW9662, or PD146176 for 20 hours after which efferocytosis assays were performed as in “Efferocytosis assay.” Data represent means plus or minus SEM; N = 6 experiments. * indicates P value less than or equal to .01 compared with untreated WT; #, P value less than or equal to .005 compared with IL-4–treated X-CGD. (B) RPMØs, either untreated or treated with 10 ng/mL IL-4 for 20 hours, were analyzed for protein expression by Western blot. (C) RPMØs were treated for 20 hours with either IL-4, 12-HETE, GW9662, or PD146176 or combinations as indicated before efferocytosis assays were performed. Data represent means plus or minus SEM; N = 5 experiments. *P ≤ .005 compared with untreated X-CGD; #P ≤ .005 compared with 12-HETE–treated X-CGD. (D) Assay was performed as in panel A, except that IgG-opsonized Jurkat T cells were used as targets. Data represent means plus or minus SEM; N = 3 experiments. (E) RPMØs were plated for 24 hours and then treated for 20 hours as indicated in panel A, lifted from the plate, fixed, stained, and analyzed by flow cytometry for CD36. Data represent means plus or minus SEM; N = 3 experiments. *P ≤ .01 compared with untreated WT; #P ≤ .005 compared with untreated X-CGD; and ΔP ≤ .005 compared with IL-4–treated X-CGD. Significant differences demonstrated in Figures 1–2 were maintained but not designated for clarity.