The balance between intrahepatic IL-17+ T cells and Foxp3+ regulatory T cells plays an important role in HBV-related end-stage liver disease

Twenty-six patients with chronic HBV -related liver failure (CLF), thirty-one patients with acute on chronic HBV-related liver failure (ACLF) and twelve normal controls were enrolled in our study. The expressions of IL-17, Foxp3, CD4, CD8 and perforin in liver tissue were measured by immunochemistry for the evaluation of liver-infiltrating lymphocytes. The frequency of liver IL-17+ T cells on liver inflammatory cells and their proportion in the total CD4+ T cell population increased markedly in the ACLF group, while the frquency of Foxp3+ T cells and their proportion in the total CD4+ T cell population did not show a significant difference in the two HBV infection groups. In addition, the ACLF group showed a dramatically higher IL-17+ /Foxp3+ ratio than the CLF group. CD4+ T cells increased significantly in the liver of patients with ACLF, compared with those in the liver of patients with CLF.Our findings suggest that intrahepatic IL-17+ T cells play an important role in the development of chronic HBV and that the imbalance between IL-17+ and Foxp3+ T cells in the liver may lead to progression of the disease but the mechanism should be further explored.Chronic hepatitis B (CHB) infection affects over 350 million individuals worldwide. It has become a global health problem due to its manifestation as chronic liver failure (CLF), acute on chronic liver failure (ACLF), liver cirrhosis (LC), and primary hepatocellular carcinoma (HCC)[1,2]. Hepatitis B virus (HBV) is preferentially hepatotropic, not directly cytopathic, and elicits liver diseases of different severity [3]. HBV may also cause sustained liver tissue damage through different pathways, including perforin-mediated cytotoxicity and Fas ligand/Fas-mediated apoptosis, when antiviral immunity is not vigorous enough to clear the virus [4]. CD8 + T cells are the main effector cells for the elimination of HBV [5]. Thus, the hepatocellular injuries caused by HBV infection are predominantly immune-mediated [1,2]. Stud