B7‐H1 expression is upregulated in peripheral blood CD14+ monocytes of patients with chronic hepatitis B virus infection, which correlates with higher serum IL‐10 levels

Abstract

Summary. Chronicity in hepatitis B virus (HBV) infection is maintained by increased type 2 T‐helper cell response, possibly because of increased interleukin‐10 (IL‐10) productions. B7‐H1 can negatively regulate T‐cell responses via its receptor, programmed death 1. Ligation of B7‐H1 to T‐cells can result in the preferential secretion of IL‐10. In this study, we investigated whether there was an upregulated expression of B7‐H1 in peripheral blood mononuclear cells in patients chronically infected by HBV and further explored the correlation between B7‐H1 expression and serum interleukin 2, interferon‐γ, IL‐10, HBeAg, alanine aminotransferase (ALT) levels and viral load. Fifty‐five patients with chronic HBV infection and 20 healthy controls (HCs) were enrolled in the present study. The results showed that in patients with chronic hepatitis B CD14+ monocytes but not CD3+ and CD19+ cells had a significantly increased expression of B7‐H1 compared with HCs, which positively correlates with serum IL‐10 levels and the presence of HBeAg and negatively correlates with serum ALT levels. In conclusion, chronic HBV patients harbour an increased B7‐H1 expression in CD14+ monocytes compared with controls, which may be responsible for the increased serum IL‐10 levels. This might be an important way by which HBV evades an adequate immune response, leading to viral persistence and disease chronicity.

Part of CIRS Nexus · Curated by Lauren Lowenstein, The Biotoxin Lady

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