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. 2017 May 8;8:525. doi: 10.3389/fimmu.2017.00525

Figure 1.

Figure 1

Role of underlying cytomegalovirus (CMV) infection in chronic viral hepatitis infections with respect to effects of natural killer (NK) cell differentiation and killer-cell immunoglobulin-like receptor (KIR) expression. (A) Representative staining of differentiation-associated receptors on CD56dim NK cells. Data shown from total lymphocytes have CD3, CD4, CD14, CD19, and dead cell marker positive cells excluded. (B) Expression of NKG2A, CD57, NKG2C, KIR2DL1, KIR2DL3, and KIR3DL1 on CD56dim NK cells in CMV seronegative (CMV−) or seropositive (CMV+) individuals, irrespective of hepatitis status; CMV− n = 9 and CMV+ n = 79. Statistical analysis performed with Mann–Whitney test. (C) Expression of NKG2A, CD57, NKG2C, KIR2DL1, KIR2DL3, and KIR3DL1 on CD56dim NK cells in CMV seropositive individuals split into healthy (n = 23) and hepatitis virus infected [n = 20, 12, and 24 for hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV), respectively]. Statistical analysis performed with Kruskal–Wallis test and Dunn’s multiple comparison. Gray bar indicates median. *p < 0.05.