In the present study, we investigated the phenotypes and functions of circulating CXCR5+CD4+ T cells in patients with chronic HBV infection and explored the relationship between circulating CXCR5+CD4+ T cells and HBeAg seroconversion. Enzalutamide datasheet One hundred and two patients with chronic HBV infection were recruited at Nanfang Hospital (Guangzhou, China) for the cross-sectional study. Patients were classified into immune tolerant carrier (IT; n = 20), HBeAg-positive CHB (n = 47), and inactive carrier (IC; n = 35) groups according to American Association for the Study of Liver Diseases guidelines.[1] Thirty-eight healthy

controls (HCs) were enrolled. Autophagy Compound Library chemical structure Forty-two patients with HBeAg-positive CHB from Nanfang Hospital who participated in a clinical trial of telbivudine were

studied longitudinally. Twenty milliliters of heparinized blood were collected at week 0, 12, 24, and 52 after starting telbivudine treatment. Subjects were classified into either a complete response (CR; n = 16) group, if they had undergone HBeAg seroconversion and achieved serum HBV DNA level less than 300 copies/mL by week 52, or a noncomplete response (NCR; n = 26) group, if serum HBV DNA was reduced, but HBeAg remained positive. All patients in both groups achieved normal alanine aminotransferase (ALT) levels by week 52. Fifty milliliters of Dichloromethane dehalogenase heparinized blood were taken for in vitro studies from another 20 CHB patients enrolled in the same clinical trial after 52 weeks of telbivudine therapy. Patients were divided into CR (n = 10) and NCR (n = 10) groups according to the aforementioned criteria. In addition, spleen tissues and 5 mL of matched heparinized blood were obtained from 10 patients who underwent splenectomy

resulting from HBV-related liver cirrhosis-induced hypersplenism. Exclusion criteria for these studies were coinfection with hepatitis A virus, hepatitis C virus (HCV), hepatitis D virus, hepatitis E virus, and human immunodeficiency virus. Patients with primary biliary cirrhosis, primary hepatocellular carcinoma, and autoimmune diseases were also excluded. These studies were conducted according to Declaration of Helsinki guidelines and were approved by the ethical committee of Nanfang Hospital. Written informed consent was obtained from all subjects. Serological assays and HBV DNA quantitation assays were performed as previously described.[12] The lowest detection limit for HBV DNA is 300 copies/mL. The normal range for serum ALT level is 0-40 U/L. Cells were stimulated in vitro with the following reagents: phorbol-12-myristate-13-acetate (PMA; Sigma-Aldrich, St.