Influence of congenital human cytomegalovirus infection and the NKG2C genotype on NK‐cell subset distribution in children

Human cytomegalovirus (HCMV) has been reported to reshape the NK‐cell receptor (NKR) distribution, promoting an expansion of CD94/NKG2C+ NK and T cells. The role of NK cells in congenital HCMV infection is ill‐defined. Here we studied the expression of NKR (i.e., NKG2C, NKG2A, LILRB1, CD161) and the...

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Published in:European journal of immunology Vol. 42; no. 12; pp. 3256 - 3266
Main Authors: Noyola, Daniel E., Fortuny, Claudia, Muntasell, Aura, Noguera‐Julian, Antoni, Muñoz‐Almagro, Carmen, Alarcón, Ana, Juncosa, Teresa, Moraru, Manuela, Vilches, Carlos, López‐Botet, Miguel
Format: Journal Article
Language:English
Published: Germany Wiley Subscription Services, Inc 01.12.2012
Subjects:
Antigens, Differentiation - biosynthesis
Antigens, Differentiation - genetics
Antigens, Differentiation - immunology
Cells
Children & youth
Congenital infection
Cytomegalovirus
Cytomegalovirus - genetics
Cytomegalovirus - immunology
Cytomegalovirus Infections - blood
Cytomegalovirus Infections - congenital
Cytomegalovirus Infections - genetics
Cytomegalovirus Infections - immunology
Female
Gene Deletion
Gene Dosage - immunology
Gene Expression Regulation - genetics
Gene Expression Regulation - immunology
Genotype & phenotype
Homeostasis - genetics
Homeostasis - immunology
Human cytomegalovirus
Humans
Immunology
Infant
Infant, Newborn
Infections
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Lymphocyte Count
Male
NK Cell Lectin-Like Receptor Subfamily C - biosynthesis
NK Cell Lectin-Like Receptor Subfamily C - immunology
NK cells
NKG2C
ISSN:0014-2980, 1521-4141, 1521-4141
Online Access:Get full text
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Summary:Human cytomegalovirus (HCMV) has been reported to reshape the NK‐cell receptor (NKR) distribution, promoting an expansion of CD94/NKG2C+ NK and T cells. The role of NK cells in congenital HCMV infection is ill‐defined. Here we studied the expression of NKR (i.e., NKG2C, NKG2A, LILRB1, CD161) and the frequency of the NKG2C gene deletion in children with past congenital infection, both symptomatic (n = 15) and asymptomatic (n = 11), including as controls children with postnatal infection (n = 11) and noninfected (n = 20). The expansion of NKG2C+ NK cells in HCMV‐infected individuals appeared particularly marked and was associated with an increased number of LILRB1+ NK cells in cases with symptomatic congenital infection. Increased numbers of NKG2C+, NKG2A+, and CD161+ T cells were also associated to HCMV infection. The NKG2C deletion frequency was comparable in children with congenital HCMV infection and controls. Remarkably, the homozygous NKG2C+/+ genotype appeared associated with increased absolute numbers of NKG2C+ NK cells. Moreover, HCMV‐infected NKG2C+/+ children displayed higher absolute numbers of NKG2A+ and total NK cells than NKG2C+/− individuals. Our study provides novel insights on the impact of HCMV infection on the homeostasis of the NK‐cell compartment in children, revealing a modulatory influence of NKG2C copy number.
Bibliography:See accompanying Commentary
http://dx.doi.org/10.1002/eji.201243050
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ISSN:0014-2980
1521-4141
1521-4141
DOI:10.1002/eji.201242752