Cutting edge: NKG2C(hi)CD57+ NK cells respond specifically to acute infection with cytomegalovirus and not Epstein-Barr virus

• Published in: The Journal of immunology (1950) 2014-05, Vol.192 (10), p.4492-4496
• Main Authors: Hendricks, Deborah W, Balfour, Jr, Henry H, Dunmire, Samantha K, Schmeling, David O, Hogquist, Kristin A, Lanier, Lewis L
• Format: Article
• Language: English
• Subjects: CD57 Antigens - immunology; Cells, Cultured; Cytomegalovirus - immunology; Cytomegalovirus Infections - immunology; Cytomegalovirus Infections - pathology; Epstein-Barr Virus Infections - immunology; Epstein-Barr Virus Infections - pathology; Female; Herpesvirus 4, Human - immunology; Humans; Killer Cells, Natural - cytology; Killer Cells, Natural - immunology; Killer Cells, Natural - pathology; Longitudinal Studies; Male; NK Cell Lectin-Like Receptor Subfamily C - immunology; NK Cell Lectin-Like Receptor Subfamily D - immunology
• ISSN: 1550-6606
• DOI: 10.4049/jimmunol.1303211

CMV induces the expansion of a unique subset of human NK cells expressing high levels of the activating CD94-NKG2C receptor that persist after control of the infection. We investigated whether this subset is CMV specific or is also responsive to acute infection with EBV. We describe a longitudinal study of CMV(-) and CMV(+) students who were acutely infected with EBV. The NKG2C(hi) NK subset was not expanded by EBV infection. However, EBV infection caused a decrease in the absolute number of immature CD56(bright)CD16(-) NK cells in the blood and, in CMV(+) individuals, induced an increased frequency of mature CD56(dim)NKG2A(+)CD57(+) NK cells in the blood that persisted into latency. These results provide further evidence that NKG2C(+) NK cells are CMV specific and suggest that EBV infection alters the repertoire of NK cells in the blood.