These authors contributed equally to this work.
HBcAg-Specific IL-21-Producing CD4+ T Cells are Associated with Relative Viral Control in Patients with Chronic Hepatitis B
Article first published online: 27 OCT 2013
© 2013 John Wiley & Sons Ltd
Scandinavian Journal of Immunology
Volume 78, Issue 5, pages 439–446, November 2013
How to Cite
Li, L., Liu, M., Cheng, L.-W., Gao, X.-Y., Fu, J.-J., Kong, G., Feng, X. and Pan, X.-C. (2013), HBcAg-Specific IL-21-Producing CD4+ T Cells are Associated with Relative Viral Control in Patients with Chronic Hepatitis B. Scandinavian Journal of Immunology, 78: 439–446. doi: 10.1111/sji.12099
- Issue published online: 27 OCT 2013
- Article first published online: 27 OCT 2013
- Accepted manuscript online: 20 AUG 2013 04:37AM EST
- Manuscript Accepted: 5 AUG 2013
- Manuscript Received: 25 MAR 2013
- National Grand Program on Key Infectious Disease of China. Grant Number: 2012ZX10002007
- Doctoral Program Construction of Higher Education in China. Grant Number: 53410903
Function exhaustion of specific cytotoxic CD8+ T cell in chronic virus infection partly results from the low levels of CD4 help, but the mechanisms by which CD4 help T cell required to control hepatitis B virus infection are not well understood. In this study, we investigated the role of interleukin-21-producing CD4+ T cell response in viral control of hepatitis B virus infection. HBcAg-specific interleukin-21-producing CD4+ T cells in blood were detected in patients with hepatitis B virus infection. Patients with acute hepatitis B had greater HBcAg-specific interleukin-21-producing CD4+ T cells in blood compared with chronic hepatitis B patients, and there was no statistical significance between immune active chronic hepatitis B patients and inactive healthy carrier patients for these cells, whereas frequencies of these cells negatively correlated with HBV DNA levels but positively correlated with HBc18-27-specific IFN-γ-producing CD8+ T cells. Moreover, interleukin-21 sustained HBc18-27-specific CD8+ T cells in vitro, and interleukin-21 production by HBcAg-specific IL-21-producing CD4+ T cells of acute hepatitis B patients enhanced IFN-γ and perforin expression by CD8+ T cells from chronic hepatitis B patients. Our results demonstrate that HBcAg-specific interleukin-21-producing CD4+ T cell responses might contribute to viral control by sustaining CD8+ T cell antiviral function.