To investigate the relationship among the expression of programmed death receptor 1 (PD-1) in peripheral blood T lymphocytes in patients with chronic hepatitis B (CHB), hepatitis B virus (HBV) DNA load and the amount of alanine aminotransferase (ALT) level.

From January 2017 to March 2018, a total of 118 patients with CHB who were treated in the Affiliated Hospital of Inner Mongolia Medical University were divided into three groups according to different immune status, which were hepatitis B antigen (HBeAg) negative group (25 cases), immune activation group (67 cases) and immune tolerance group (26 cases); while 50 healthy physical examination persons in our hospital were selected as control group. Liver function was detected by automatic biochemical analyzer, HBV core antibody (HBcAb), HBV surface antigen (HBsAg), hepatitis B e antibody (HBeAb), HBeAg and hepatitis B surface antibody (HBsAb) were detected by ELISA, and HBV DNA load was detected by fluorescence quantitative PCR. The expression of PD-1, CD8⁺ T and CD4⁺ T lymphocytes in serum were detected by flow cytometry.

In patients of immune activated group and HBeAg negative group, the expression of PD-1 CD8⁺ T and CD4⁺ T lymphocytes in serum were (7.48 ± 1.76)%, (7.48 ± 1.76)% and (10.58 ± 1.95)%, (8.38 ± 1.85)%, respectively, all significantly higher than those of control group [(3.22 ± 1.53)% and (4.05 ± 1.76)%] and immune tolerance group [(4.26 ± 1.89)% and (3.86 ± 1.89)%], with significant differences (F = 12.084, P = 0.015; F = 13.297, P = 0.032). The HBV DNA load was (7.02 ± 1.13) log₁₀ copies/ml in immune activation group and (5.77 ± 1.25) log₁₀ copies/ml in HBeAg negative group, significantly lower than that of the immune tolerance group [(8.18 ± 1.08) log₁₀ copies/ml], with significant difference (F = 11.652, P = 0.006). The levels of serum ALT and total bilirubin in immune activated group and HBeAg negative group were (193.02 ± 7.39) IU/ml, (50.06 ± 2.18) mmol/L and (179.14 ± 7.62) IU/ml, (43.65 ± 2.27) mmol/L, respectively, all signifcantly higher than those of the control group [(12.71 ± 6.19) IU/ml and (13.07 ± 2.19) mmol/L] and immune tolerance group [(23.19 ± 6.82) IU/ml] and (16.54 ± 2.30) mmol/L, with significant differences (F = 10.906, P = 0.027; F = 9.583, P = 0.019). Pearson correlation analysis showed that there was no correlation between the levels of CD8⁺ T, CD4⁺ T of PD-1 in serum and the level of ALT in patients of immune tolerance group, immune activation group and HBeAg negative group (r =-0.170, 0.046, 0.068, -0.231, 0.048, 0.005; P = 0.443, 0.750, 0.761, 0.292, 0.709, 0.912), and no correlation with serum HBV DNA load (r =-0.049, 0.107, 0.104, -0.301, 0.019, 0.279; P = 0.810, 0.440, 0.681, 0.201, 0.883, 0.221).

There were correlation between the immune status of CHB patients and the PD-1 expression on the surface of T cells in serum. The damage of liver inflammation has an important effect on the expression of PD-1, but HBV DNA load is not the main factor.