Fig. 1.

Poly(inosinic:cytidylic) acid [poly(I:C)] activates proinflammatory signaling and inflammatory gene expression in the absence of Toll-like receptor (TLR) 3. A: naïve peritoneal exudate cells, isolated from wild-type or TLR3^−/− mice, were treated for 15 and 30 min with poly(I:C) and harvested, and ERK, JNK, and p38 phosphorylation (p-) and IκBα degradation were detected by Western blot analysis. Total p38 is shown as a loading control. B: macrophages were treated for 24 h with poly(I:C) and IFN-γ and harvested, and inducible nitric oxide synthase (iNOS) and pro-IL-1β were detected by Western blot analysis. GAPDH is shown as a loading control. C: macrophages were isolated from wild-type or TLR3^−/− mice and treated for 16 h with poly(I:C). RNA was isolated, and IFN-α mRNA accumulation was quantified by real-time PCR and normalized to actin mRNA. Results are representative (A and B) or means ± SE (C) of 3 independent experiments. *P < 0.05 vs. TLR^−/−. COX-2, cyclooxygenase-2.