000445320_sm_Figure.pdf (311.8 kB)
Supplementary Material for: Cytomegalovirus-Infected Primary Endothelial Cells Trigger NKG2C+ Natural Killer Cells
figure
posted on 2016-05-10, 15:08 authored by Zakia Djaoud, Raphaëlle Riou, Pierre-Jean Gavlovsky, Souad Mehlal, Céline Bressollette, Nathalie Gérard, Katia Gagne, Béatrice Charreau, Christelle RetièreAmong innate cells, natural killer (NK) cells play a crucial role in the
defense against cytomegalovirus (CMV). In some individuals, CMV
infection induces the expansion of NKG2C+ NK cells that persist after control of the infection. We have previously shown that KIR2DL+ NK cells, in contrast to NKG2C+
NK cells, contribute to controlling CMV infection using a CMV-infected
monocyte-derived dendritic cell (MDDC) model. However, the nature of
CMV-infected cells contributing to the expansion of the NKG2C+ NK cell subset remains unclear. To gain more insight into this question, we investigated the contribution of NKG2C+
NK cell activation by CMV-infected primary human aortic endothelial
cells (EC) isolated from kidney transplant donors, which constitutively
express the human leukocyte antigen (HLA)-E molecule. Here, we show
that, although classic HLA class I expression was drastically
downregulated, nonclassic HLA-E expression was maintained in
CMV-infected EC. By comparing HLA expression patterns in CMV-infected
EC, fibroblasts and MDDC, we demonstrate a cell-dependent modulation of
HLA-E expression by CMV infection. NKG2C+ NK cell
degranulation was significantly triggered by CMV-infected EC regardless
of the nature of the HLA-E allele product. EC, predominantly present in
vessels, may constitute a privileged site for CMV infection that drives a
‘memory' NKG2C+ NK cell subset.