title: Influence of congenital human cytomegalovirus infection and the NKG2C genotype on NK-cell subset distribution in children.
abstract: 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.
authors.affiliation: Department of Microbiology, Universidad Autónoma de San Luis Potosí, San Luis Potosí, México.
authors.forename: Daniel E
authors.initials: DE
authors.lastname: Noyola
authors.forename: Claudia
authors.initials: C
authors.lastname: Fortuny
authors.forename: Aura
authors.initials: A
authors.lastname: Muntasell
authors.forename: Antoni
authors.initials: A
authors.lastname: Noguera-Julian
authors.forename: Carmen
authors.initials: C
authors.lastname: Muñoz-Almagro
authors.forename: Ana
authors.initials: A
authors.lastname: Alarcón
authors.forename: Teresa
authors.initials: T
authors.lastname: Juncosa
authors.forename: Manuela
authors.initials: M
authors.lastname: Moraru
authors.forename: Carlos
authors.initials: C
authors.lastname: Vilches
authors.forename: Miguel
authors.initials: M
authors.lastname: López-Botet
mesh_terms: D000943:Antigens, Differentiation / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D003587:Cytomegalovirus / Q000235:genetics / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000097:blood / Q000151:congenital* / Q000235:genetics / Q000276:immunology*; D005260:Female; D017353:Gene Deletion; D018628:Gene Dosage / Q000276:immunology; D005786:Gene Expression Regulation / Q000235:genetics / Q000276:immunology*; D006706:Homeostasis / Q000235:genetics / Q000276:immunology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D018655:Lymphocyte Count; D008297:Male; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000096:biosynthesis / Q000276:immunology*
chemical_list: D000943:Antigens, Differentiation; C527059:KLRC2 protein, human; D055654:NK Cell Lectin-Like Receptor Subfamily C