FIG. 3.
The proinflammatory effect of functional inhibition of surface-expressed TLR3 in response to poly(IC) stimulation and RV infection. (A) Cells were infected for 1 h with RV-16 (MOI of 1), UV-inactivated RV-16 (MOI of 1), or the same volume of filtered RV-16. The amounts of IL-6, CXCL8, and CCL5 secreted into the supernatants were quantified after 24 h. Data for panel A are presented as the concentrations of proinflammatory mediator in the supernatants. (B) Cells were pretreated for 1 h with anti-TLR3 or isotype control antibodies before stimulation with 0.1 μg/ml poly(IC) [antibodies were replaced 1 h after the initial application of poly(IC)]. The amounts of IL-6, CXCL8, and CCL5 secreted into the supernatants were quantified after 24 h. (C) Cells were pretreated with the antibodies as described for panel B before being infected for 1 h with RV-16 (MOI of 1). The antibodies were then replaced, and IL-6, CXCL8, and CCL5 were quantified 24 h postinfection. Data for panels B and C are presented as percentage release compared to stimulated/infected cells without antibody. For panel A data are significantly different (***) between RV-16- and UV-RV-16-infected cells at P < 0.001 (n = 5). For panels B and C, values are significantly different between stimulated/infected cells ± anti-TLR3 antibody at P < 0.01 (*) and P < 0.001 (***) (n = 5).