Skip to main content
. 2017 Sep 12;67(11):2035–2044. doi: 10.1136/gutjnl-2017-314098

Figure 7.

Figure 7

HBV-induced NK cells via monocytes inhibit autologous CD4+ and CD8+ T cells activation in IL-10 dependent manner. NK cells repurified from monocytes/NK cells coculture with or without HBsAg/HBVcc were cocultured with CFSE-labelled autologous T cells and stimulated with PHA in presence of anti IL-10 antibody. (A–C) CD4+ and CD8+ T cell proliferation was examined by flow cytometry. (D) The supernatants of NK/T cell coculture were collected for IFN-γ detection by ELISA. To investigate the regulatory effect of NK cells on HBV-specific T cell response, monocytes, NK cells and T cells were purified from patients with CHB. T cells were cocultured with autologous DCs loaded with either HBsAg or HEV-ORF2 protein in the presence of NK cells, which were repurified from monocyte/NK cell coculture with or without HBsAg/HBVcc. (E–G) CD4+ and CD8+ T cell proliferation was examined by flow cytometry. (H–J) IFN-γ expression of CD4+ and CD8+ T cells were examined by intracellular cytokine staining. Shown is one of five representative experiments. The bars represent the SEM. *p<0.05. CHB, chronic HBV infection; DCs, dendritic cells; HBsAg, hepatitis B surface antigen; HBVcc, cell culture of HBV; HEV-ORF2, hepatitis E virus open reading frame 2; IL, interleukin; NK, natural killer.