title: Natural killer cell receptor repertoire and their ligands, and the risk of CMV infection after kidney transplantation.
abstract: Cytomegalovirus (CMV) infection is the most common viral complication after solid organ transplantation (SOT). Whilst current immunosuppression is known to impair antiviral-specific T-cell immunity in SOT, a potential role for natural killer (NK) cells not affected by immunosuppressive therapy remains to be determined. To address this, we compared the genotype of the NK immunoglobulin-like receptor (KIR) genes and their HLA cognate ligands to the rate of CMV infection in 196 kidney transplant recipients. We have shown that the absence of the HLA-C ligand for inhibitory KIR and the presence of activating KIR genes in the recipients were both associated with a lower rate of CMV infection after transplantation. In a cohort of 17 recipients with acute CMV infection, NK cells were phenotyped over a period of time after diagnosis by their expression profile of C-type lectin receptors and capacity to secrete IFN-gamma. The increased expression of the activating C-type lectin receptors NKG2C and NKG2D was paralleled by the decreased IFN-gamma secretion during the early phase of CMV infection. In conclusion, our findings suggest that KIR/HLA genotype and expression of NKG2C and NKG2D might play a significant role in regulating NK cell function and anti-CMV immunity after kidney transplantation.
authors.affiliation: Service of Nephrology, Geneva University Hospital and Medical School, Switzerland.
authors.forename: K
authors.initials: K
authors.lastname: Hadaya
authors.forename: C
authors.initials: C
authors.lastname: de Rham
authors.forename: C
authors.initials: C
authors.lastname: Bandelier
authors.forename: C
authors.initials: C
authors.lastname: Bandelier
authors.forename: S
authors.initials: S
authors.lastname: Ferrari-Lacraz
authors.forename: S
authors.initials: S
authors.lastname: Jendly
authors.forename: T
authors.initials: T
authors.lastname: Berney
authors.forename: L
authors.initials: L
authors.lastname: Buhler
authors.forename: L
authors.initials: L
authors.lastname: Kaiser
authors.forename: J D
authors.initials: JD
authors.lastname: Seebach
authors.forename: J M
authors.initials: JM
authors.lastname: Tiercy
authors.forename: P Y
authors.initials: PY
authors.lastname: Martin
authors.forename: J
authors.initials: J
authors.lastname: Villard
mesh_terms: D000328:Adult; D003587:Cytomegalovirus / Q000276:immunology; D003586:Cytomegalovirus Infections / Q000453:epidemiology* / Q000276:immunology; D005260:Female; D005838:Genotype; D015236:HLA-C Antigens / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D016030:Kidney Transplantation / Q000276:immunology; D007694:Killer Cells, Natural / Q000502:physiology; D037181:Lectins, C-Type / Q000235:genetics / Q000378:metabolism*; D008024:Ligands; D008297:Male; D008875:Middle Aged; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000235:genetics / Q000378:metabolism; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000235:genetics / Q000378:metabolism; D011183:Postoperative Complications; D054340:Receptors, KIR / Q000235:genetics / Q000378:metabolism; D055607:Receptors, Natural Killer Cell / Q000235:genetics / Q000378:metabolism*; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D015236:HLA-C Antigens; C527059:KLRC2 protein, human; C527085:KLRK1 protein, human; D037181:Lectins, C-Type; D008024:Ligands; D055654:NK Cell Lectin-Like Receptor Subfamily C; D055655:NK Cell Lectin-Like Receptor Subfamily K; D054340:Receptors, KIR; D055607:Receptors, Natural Killer Cell; D007371:Interferon-gamma