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. Author manuscript; available in PMC: 2013 Oct 19.
Published in final edited form as: J Immunol. 2011 Jun 10;187(2):887–896. doi: 10.4049/jimmunol.1003737

Figure 2.

Figure 2

MHV68 suppresses TLR signaling in cDCs. A and B, GM-CSF–derived DCs from wild-type (white bars) and MyD88−/− (black bars) mice were treated with CpG ODN or infected with MCMV (MOI 1) or MHV68 (indicated MOIs). Levels of IL-12p40 (A) and IFN-I (B) secreted into the supernatant were determined 20 h postinfection by ELISA or ISRE bioassay, respectively. C and D, GM-CSF–derived DCs were infected or not with MHV68 gM–eGFP at MOI 1 for 2 h and subsequently treated with LPS or CpG or left untreated. Cytokine production in infected cells was assessed by IL-12p40 ELISA of supernatants (C) or by intracellular cytokine staining for IL-12 (D, data shown is gated on CD11c+, CD11b+ cells). Percentages of IL-12+ cells in either infected (GFP+) or uninfected and latently infected (GFP−) cells after LPS and CpG stimulation are presented graphically on the left. Average and SD of triplicate wells are shown (data are representative of multiple independent experiments).