Decreased frequency of a novel T-lymphocyte subset, CD3 CD4 CD7 CD57 T cells, in hepatitis B virus-related end-stage liver disease might contribute to disease progression.

CD7 and CD57 are related to the differentiation and functional stages of CD8 T cells. However, the role of their combined presence in CD8 T cells in patients with chronic hepatitis B virus (HBV) infection, especially those with end-stage liver disease, remains unclear. Blood samples from healthy volunteers and patients with chronic hepatitis B were analyzed via Luminex assay and ELISA to measure plasma cytokine levels. Further, recombinant IL-22 was used to stimulate peripheral blood mononuclear cells from healthy volunteers, and the frequency of CD3 CD4 CD7 CD57 T cells and apoptosis rates were investigated via flow cytometry. Patients with end-stage liver disease, particularly those with acute to chronic liver failure, showed decreased CD3 CD4 CD7 CD57 T cell frequency. Furthermore, the prevalence of CD3 CD4 CD7 CD57 T cells was negatively correlated with disease severity, prognosis, and complications (ascites). We also observed that IL-22 promoted apoptosis and brought about a decrease in the number of CD3 CD4 CD7 CD57 T cells in a dose-dependent manner. CD3 CD4 CD7 CD57 T cells displayed a B and T lymphocyte attenuator (BTLA) CD25 CD127 immunosuppressive phenotype and showed low interferon-γ, tumor necrosis factor-α, granzyme A, and perforin expression levels. The present findings will elucidate the pathogenesis of HBV-related end-stage liver disease and aid the identification of novel drug targets.