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- Title
Selective functional deficit in dendritic cell – T cell interaction is a crucial mechanism in chronic hepatitis B virus infection.
- Authors
Zheng, B. J.; Zhou, J.; Qu, D.; Siu, K. L.; Lam, T. W.; Lo, H. V.; Lee, S. S.; Wen, Y. M.
- Abstract
A defect in specific T cell immunity has long been assumed to be the central mechanism of persistent Hepatitis B virus (HBV) infection. Recent studies on HBV transgenic mice have suggested, however, that functional deficit of dendritic cells (DC) was an underlying cause for the T cell dysfunction. The functions of monocyte-derived DC were determined by studying 75 subjects that included chronic hepatitis B patients with low or high HBV load; antibody to hepatitis B surface antigen (anti-HBs) positive individuals who had recovered completely from previous acute HBV infection; healthy donors who had received hepatitis B vac- cination and were anti-HBs positive; and immunologically naive to HBV or the vaccine individual. Impaired interactions between monocyte-derived DC and T cells were shown in chronic HBV infection patients, especially in those with active virus replication. The dysfunctions included: (i) failure of DC to increase human leukocyte antigen (HLA-II), B7 expression and interleukin-12 secretion in responses to hepatitis B surface antigen (HBsAg), (ii) defective induction of T cell proliferative response to HBsAg, (iii) failure to activate T cells to produce cytokines and (iv) deficit in the induction of antigen specific cytotoxic T lymphocytes (CTL5). In vitro treatment of DC with tumour necrosis factor-x improved HLA-II and B7 expression, as well as Th cell and CTL responses. It is concluded that defective DC-T cell interactions may account for the specific T cell immune defects in chronic HBV infection. Immunotherapy that aims at restoring DC functions could offer a new opportunity for effectively managing persistent HBV infections.
- Subjects
PREVENTIVE medicine; HEPATITIS B; MEDICAL care; T cells; ANTIGENS; IMMUNOGLOBULINS
- Publication
Journal of Viral Hepatitis, 2004, Vol 11, Issue 3, p217
- ISSN
1352-0504
- Publication type
Article
- DOI
10.1111/j.1365-2893.2004.00497.x