A Role for Host Activation-Induced Cytidine Deaminase in Innate Immune Defense against KSHV
Figure 2
KSHV infection leads to upregulation of NKG2D ligands.
(A) Tonsillar cells were infected by co-culture with reactivated iSLK.219 cells. CD19+ population was enriched and subsequently sorted for infected, GFP+ and uninfected, GFP− cells. Relative levels of four detected NKG2D transcripts were measured by qRT-PCR. Shown are mean values ± SD from at least three patients (*p<.01 by two-tailed, paired student t-test). (B) CD19+ tonsillar B cells were assessed for surface expression of MICB (top panel) and ULBP2 (bottom panel) by flow cytometry. Infected, GFP+ cells are depicted in red and uninfected, GFP− cells in filled gray; isotype control is shown in dashed black. (C) Infected cells were treated with DNA damage inhibitors, caffeine (middle panel) and SB218078 (right panel) for the duration of the infection. Infected, drug-treated B cells are shown in blue and uninfected drug-treated cells in thin black as compared to vehicle controls depicted same as in (B). (D) Tonsillar B cells were sorted for infected, GFP+ and uninfected, GFP− cells. GFP−, uninfected cells were labeled with CFSE for tracking. Infected or uninfected cells were co-incubated with effector NK-92 cells at specified ratios for 5 hours and assayed for killing by flow cytometry. Percentage of dead target cells is indicated by the blue rectangular gates. All experiments presented in the figure were done on day 4 post infection.