PMID- 27116381
OWN - NLM
STAT- MEDLINE
DCOM- 20170922
LR  - 20231213
IS  - 1662-8128 (Electronic)
IS  - 1662-811X (Print)
IS  - 1662-811X (Linking)
VI  - 8
IP  - 4
DP  - 2016
TI  - Cytomegalovirus-Infected Primary Endothelial Cells Trigger NKG2C+ Natural Killer 
      Cells.
PG  - 374-85
LID - 10.1159/000445320 [doi]
AB  - Among 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.
CI  - (c) 2016 S. Karger AG, Basel.
FAU - Djaoud, Zakia
AU  - Djaoud Z
AD  - Etablissement Franx00E7;ais du Sang, ImmunoVirologie et Polymorphisme 
      Gx00E9;nx00E9;tique, Universitx00E9; de Nantes, Nantes, France.
FAU - Riou, Raphaelle
AU  - Riou R
FAU - Gavlovsky, Pierre-Jean
AU  - Gavlovsky PJ
FAU - Mehlal, Souad
AU  - Mehlal S
FAU - Bressollette, Celine
AU  - Bressollette C
FAU - Gerard, Nathalie
AU  - Gerard N
FAU - Gagne, Katia
AU  - Gagne K
FAU - Charreau, Beatrice
AU  - Charreau B
FAU - Retiere, Christelle
AU  - Retiere C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160427
PL  - Switzerland
TA  - J Innate Immun
JT  - Journal of innate immunity
JID - 101469471
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (KIR2DL1 protein, human)
RN  - 0 (KLRC2 protein, human)
RN  - 0 (NK Cell Lectin-Like Receptor Subfamily C)
RN  - 0 (Receptors, KIR2DL1)
SB  - IM
MH  - Aorta/pathology
MH  - Cell Degranulation
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Cytomegalovirus/*immunology
MH  - Cytomegalovirus Infections/*immunology
MH  - Dendritic Cells/*immunology/virology
MH  - Endothelium, Vascular/*immunology/virology
MH  - Fibroblasts/*immunology/virology
MH  - Histocompatibility Antigens Class I/genetics/metabolism
MH  - Humans
MH  - Immunologic Memory
MH  - Killer Cells, Natural/*immunology/virology
MH  - Lymphocyte Activation
MH  - Lymphocyte Subsets/*immunology/virology
MH  - NK Cell Lectin-Like Receptor Subfamily C/metabolism
MH  - Receptors, KIR2DL1/metabolism
MH  - HLA-E Antigens
PMC - PMC6738823
EDAT- 2016/04/27 06:00
MHDA- 2017/09/25 06:00
PMCR- 2016/04/27
CRDT- 2016/04/27 06:00
PHST- 2015/12/18 00:00 [received]
PHST- 2016/03/09 00:00 [accepted]
PHST- 2016/04/27 06:00 [entrez]
PHST- 2016/04/27 06:00 [pubmed]
PHST- 2017/09/25 06:00 [medline]
PHST- 2016/04/27 00:00 [pmc-release]
AID - 000445320 [pii]
AID - jin-0008-0374 [pii]
AID - 10.1159/000445320 [doi]
PST - ppublish
SO  - J Innate Immun. 2016;8(4):374-85. doi: 10.1159/000445320. Epub 2016 Apr 27.