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. 2008 May 28;82(15):7666–7676. doi: 10.1128/JVI.02274-07

FIG. 2.

FIG. 2.

Binding of anti-MHC class I and NK-inhibitory receptors to THP-1 and THP-1.ΔCprME-PAC2A cells. (A) RT-PCR of THP-1 and THP-1.ΔCprME-PAC2A cells showing the expression of the DV replicon. (B) Surface expression of MHC class I in THP-1 and THP-1.ΔCprME-PAC2A cells analyzed by flow cytometry with the pan-HLA-specific MAb W6/32. Background staining with the secondary antibody (2Ab) is presented. Mean fluorescence intensities (MFIs) were 2.5 for background staining, 242 for THP-1 cells, and 417 for THP-1.ΔCprME-PAC2A cells. Results are from one representative experiment out of three performed. (C) Binding of different receptor-Igs to THP-1 and THP-1.ΔCprME-PAC2A cells. MFIs for THP-1 and THP-1.ΔCprME-PAC2A cells were, respectively, as follows: CD99-Ig, 2.1 and 3.6; KIR2DS2-Ig, 2.3 and 2.1; KIR2DL1-Ig, 15.9 and 15.8; LIR1-Ig, 5.2 and 78.9. (D) Flow cytometry analysis of MHC class I surface expression (top) and LIR1-Ig staining (bottom) of THP-1 and IFN-γ-treated THP-1 cells. THP-1 cells were treated with 100 U/ml recombinant human IFN-γ for 36 h. Cells were then stained with W6/32 or with secondary antibody only (2Ab) or stained with LIR1-Ig. Results are from one representative experiment out of two performed.