Skip to main content
. 2021 Feb 3;9(2):363–373. doi: 10.1002/iid3.397

Figure 3.

Figure 3

Signal transduction mechanisms in poly(I:C) and IL‐13‐induced CCL5 production in BEAS‐2B cells. (A–E) Poly(I:C) and IL‐13‐induced CCL5 production was not reduced with si‐STAT6 (A) but was inhibited with the PI3K inhibitor, LY294002 (5 µM, B). (C–E) si‐IRF3 (C), and si‐JAK1 (D). The JAK1/2 inhibitor, ruxolitinib (10 µM, E), also reduced poly(I:C) and IL‐13‐induced CCL5 production. BEAS‐2B cells were pre‐incubated with siRNA for 2 days (A, C, D) or with inhibitors for 2 h (B, E), followed by stimulation with poly(I:C) (0.1 μg/ml) for 24 h. *p < .05, **p < .01, as compared to medium alone. We used student t tests (A, C, D) or one‐way ANOVA with post hoc Holm–Sidak's multiple tests to conduct selected pairwise comparisons of treatments (B, E). ANOVA, analysis of variance; CCL5, chemokine (C‐C motif) ligand 5; IL, interleukin; JAK1, Janus kinase 1; NC, negative control; PI3K, phosphoinositide 3‐kinase; pIC, poly(I:C); siRNA, small interfering RNA