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. 2015 Aug 19;89(21):10860–10867. doi: 10.1128/JVI.01627-15

FIG 3.

FIG 3

Role of TRIF-mediated signaling in IFN-β expression. (A and B) Fourteen-day-old WT or TRIF-deficient C57BL/6 mice were infected i.p. with 1.5 ×104 PFU CVA16, and then the IFN-β expression levels in the indicated tissues of infected mice were measured by qRT-PCR on days 2 (A) and 4 (B). (C and D) WT and TLR3-deficient BMDCs (C) and BMMs (D) from mice with a strain 129 background were infected with CVA16 at a multiplicity of infection of 10 (1.0 × 106 PFU/1.0 × 105 cells) for the indicated times, and the expression of IFN-β was measured by qRT-PCR. (E to G) WT and TRIF-deficient BMDCs (E), BMMs (F), and MEFs (G) from mice with a C57BL/6 background were infected with CVA16 at a multiplicity of infection of 10 (1.0 × 106 PFU/1.0× 105 cells) for the indicated times, and the expression of IFN-β was measured by qRT-PCR. Positive controls consisted of BMDCs, BMMs, and MEFs stimulated with poly(I·C) (pI:C). (H) The viral loads in infected cells from WT mice with a C57BL/6 background were examined by qRT-PCR at 0 and 6 h postinfection. (I) BMDCs and BMMs from WT mice with a C57BL/6 background were infected with live or UV-inactivated CVA16 at a multiplicity of infection of 10 (1.0 × 106 PFU/1.0 × 105 cells) for the indicated times, and the expression of IFN-β was measured by qRT-PCR. Data are shown as the mean ± SEM and are representative of those from three independent experiments (n = 3, respectively). ns, not significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001.