Fig. 3.

MAP kinases do not mediate the expression or release of IL-36γ in keratinocytes treated with low doses of poly(I:C). a HFKs were treated with vehicle (control) or with inhibitors of the EGFR (1 µM), MEK (50 µM), p38 (10 µM), PI-3 K (25 µM) or JNK (10 µM) for 3 h and then poly(I:C) (1500 ng/ml) was added for an additional 48 h and IL-36γ analyzed by western blot. IL-36γ levels were normalized to β-actin to correct for protein loading. Bars show mean ± SD, relative to controls (n = 8 experiments). b HFKs were pretreated with vehicle or inhibitor as in (a) for 3 h. Poly(I:C) (1500 ng/ml) was added as indicated, cells incubated for 96 h, and conditioned medium analyzed by ELISA for accumulated IL-36γ. Bars show mean ± SD of IL-36γ normalized to μg of cellular protein in the secreting monolayer, relative to cells treated with poly(I:C) in the absence of inhibitor (n = 8 experiments)