Fig. 2.

Induction of IL-1Ra expression by poly(I:C) is dependent on the TLR3 activation. Human FLS were treated with siRNA TLR3 (a), siRNA MDA5 (b), siRNA RIG-I (c), or siRNA negative control (NC) for 48 h. The cells were harvested and the levels of human TLR3, MDA5 and RIG-I mRNA expression were measured by real-time PCR. Downregulation of human TLR3, MDA5 and RIG-I expression are compared with siRNA NC group. Human FLS were pre-treated with siRNA TLR3 (d), siRNA MDA5 (e), siRNA RIG-I (f), or siRNA NC for 48 h and stimulated by poly(I:C) for 24 h. The culture supernatants were harvested and the concentrations of IL-1Ra were determined with ELISA. WT (341bp) and TLR3^−/− (208 bp) mice were identified by PCR (g). FLS (10⁵ cells/mL) from WT or TLR3^−/− mice were stimulated by poly(I:C) for 24 h (h). The culture supernatants were harvested and the concentrations of IL-1Ra were determined with ELISA. Results are presented as mean ± SEM (n = 5 per group) from 3 separate experiments. * p < 0.05 versus the siRNA NC group without poly(I:C; a–c) or with poly(I:C; d–f, h). MDA5, melanoma differentiation-associated protein 5; RIG-I, retinoic acid-inducible gene I; IL-1Ra, IL-1 receptor antagonist; TLR3, toll-like receptor 3.