Skip to main content
. 2017 Jul 26;6:F1000 Faculty Rev-1231. [Version 1] doi: 10.12688/f1000research.11197.1

Figure 1. Differentiation and stimulation of human natural killer (NK) cells during Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) infection.

Figure 1.

Human NK cells differentiate with acquisition of killer immunoglobulin-like receptor (KIR) expression and lose NKG2A expression upon terminal differentiation. Expression of the senescence marker CD57 removes NK cell subpopulations from this differentiation. Lytically EBV-replicating plasma cells are preferentially recognized by early differentiated NK cells via their NKG2D and DNAX accessory molecule-1 (DNAM-1) receptors, while HCMV-infected cells expand terminally differentiated NK cells via CD94/NKG2C stimulation by HCMV peptide-presenting human leukocyte antigen (HLA)-E molecules. HCMV-infected cells are targeted by these terminally differentiated NK cells after antibody opsonization.