Natural Killer Group 2A Expressed on Both Peripheral CD3 - CD56 + NK Cells and CD3 + CD8 + T Cells Plays a Pivotal Negative Regulatory Role in the Progression of Hepatitis B Virus-Related Acute-on-Chronic Liver Failure.

To explore the role of surface receptors natural killer group 2A (NKG2A) and natural killer group 2D (NKG2D) on CD3+ CD8+ T cells and CD3- CD56+ NK cells in the progression of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF), we measured the expression of NKG2A and NKG2D on the surface of these 2 types of circulating cells by flow cytometry in 3 groups. One group consists of 36 patients with chronic hepatitis B (CHB), another one consists of 22 patients with HBV-related ACLF, and the last one has 12 normal controls (NC). The experimental result indicated that there was no significant difference in the proportion of CD3+ CD8+ T cells in total lymphocytes between the 3 groups. However, the percentage of CD3- CD56+ NK cells in ACLF group was evidently higher than that in the CHB group (P < 0.05). In addition, the expression of NKG2D on CD3+ CD8+ T cells in the ACLF group was significantly lower than that in the CHB group (P < 0.05), but there were no statistically significant differences in its percentages on CD3- CD56+ NK cells between the 3 groups. The expression of NKG2A on CD3+ CD8+ T cells in the ACLF group was significantly higher than that in the NC group (P < 0.05), and on NK cells was significantly higher than that in the CHB group (P < 0.05) and NC group (P < 0.01). The increase in ratios of NKG2A to NKG2D on CD3+ CD8+ T cells and CD3- CD56+ NK cells in the ACLF group was significantly more than that in the CHB group and NC group. The results indicate that the imbalance between NKG2A and NKG2D may contribute to the progression of HBV-related ACLF mediated by CD3- CD56+ NK cells and CD3+ CD8+ T cells. Compared with NKG2D, NKG2A expressed on both peripheral CD3- CD56+ NK cells and CD3+ CD8+ T cells plays a more pivotal negative regulatory role in the progression of HBV-related ACLF.