Figure 2

EBV derived peptides upregulate HLA-E surface expression. (a) LMP1 and LMP2, (b) EBNA-1 and ENBA-2, (c) EBNA-3A, -3B and -3C encoding peptides were pulsed onto target cells. HLA-E expression was assessed the following day. Peptides that bound HLA-E induced upregulation of HLA-E (mean fluorescence intensity (MFI) values) surface expression, which is shown as relative mean fluorescence intensity (RFI) as compared to HLA-E expression in absence of peptide (No Peptide). Endogenous peptide, HLA-A03 leader peptide (white filled bar) and viral peptide, BZLF1 (checkered bars) derived from EBV were used as positive controls. The dashed grey line represents the background expression in absence of peptide (cut-off set by No Peptide) and the black dashed line represents the cut-off for the peptides considered HLA-E binders. Peptides represented by black bars were considered as binders and peptides in grey bars non-binders. Mean ± SEM of two independent experiments.