MHC Class I Molecules Exacerbate Viral Infection by Disrupting Type I Interferon Signaling

Figure 1

MHC I promotes viral infection independent of type I IFN. (a) VSV RNA replication in WT and MHC I^-/- macrophages stimulated with VSV for 6 h, as determined by real-time qPCR analysis. (b) Detection of VSV viral load by TCID₅₀ in the supernatant from WT and MHC I^-/- macrophages. (c) VSV-GFP replication in WT or MHC I^-/- macrophages after 12 h and visualized by fluorescence microscopy. (d) Flow cytometry analysis of WT and MHC I^-/- macrophages infected with VSV-GFP after 16 h. (e) Percentages and FITC MFI of GFP⁺ cells in (d). (f) VSV RNA replication in WT macrophages overexpressed with MHC I or control vectors. (g) Relative type I IFN mRNA expression in WT and MHC I^-/- macrophages at indicated times post infection. (h) Type I IFN in the supernatant of VSV-infected WT and MHC I^-/- macrophages 24 h later, analyzed by ELISA assay. (i) Intracellular IFN-β staining of WT and MHC I^-/- macrophages post VSV infection (left) and statistical MFI of IFN-β (right). Data are the of at least three independent experiments. Two-way ANOVA was adopted for statistical analysis in (a), (g), and (h). One-way ANOVA was adopted for statistical analysis in (i). Student’s -test was adopted for analysis in (e) and (f). and .

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