PMID- 21134826
OWN - NLM
STAT- MEDLINE
DCOM- 20110325
LR  - 20220408
IS  - 1499-3872 (Print)
VI  - 9
IP  - 6
DP  - 2010 Dec
TI  - Recognition of HBV antigens and HBV DNA by dendritic cells.
PG  - 584-92
AB  - BACKGROUND: Hepatitis B virus (HBV) is a hepatotropic, noncytopathic, DNA virus 
      which can cause acute and chronic infection. Viral persistence is associated with 
      a weak or absent specific immune responses to HBV, particularly the cellular 
      immune response. Dendritic cells (DCs) are professional antigen-presenting cells 
      with a unique T cell stimulatory aptitude that play a crucial role in the 
      instruction of adaptive immune responses upon infection. An impaired function of 
      DCs was suggested by recent studies to account for the T and B cell 
      hyporesponsiveness in chronic HBV infection. This review summarizes recent 
      insights into the recognition of HBV antigens by DCs. DATA SOURCES: Studies were 
      identified by searching MEDLINE and/or PubMed for articles using the key words 
      "hepatitis B virus (HBV)", "dendritic cells", "C-type lectins", "mannose 
      receptor", "toll-like receptor", and "dendritic cell-specific 
      intercellular-adhesion-molecule-3 grabbing nonintegrin (DC-SIGN)" up to December 
      2009. Additional papers were identified by a manual search of the references from 
      the key articles. RESULTS: DCs play an important role in the progress of 
      hepatitis B, especially in the recognition of HBV. There are three main ways of 
      recognition of HBV antigens by DCs. First, HBV DNA can be recognized by DCs 
      through toll-like receptor 9 (TLR9) which activates the NF-kappaB signal pathway and 
      p38 MAPK to up-regulate the expression of interferon (IFN) regulatory factor 7 
      (IRF-7) in a manner independent of type I IFN signaling, resulting in secretion 
      of type I IFN and inflammatory cytokines, and induction of DC maturation and the 
      adaptive immune response. Second, HBc/HBeAg cannot be recognized by DCs, but DNA 
      or ssRNA encapsulated within HBcAg can be internalized by DCs through TLRs. 
      Third, HBsAg can be internalized by DCs through the mannose receptor, which lacks 
      the ability to induce DC maturation without the assistance of DC-SIGN. Meanwhile, 
      there is some cross-talk among the three mechanisms, which induces an effective 
      anti-viral response or HBV persistence. CONCLUSIONS: On the basis of these 
      recognition processes, methods have been used to enhance the efficacy of DC-based 
      vaccine against HBV and have been useful in the clinical application of HBV 
      vaccine therapy. But the interactions between HBV antigens/HBV DNA and DCs are 
      not clear, and cross-talk between TLRs and various ligands makes HBV antigen 
      recognition by DCs more complicated. More efforts should be made to define the 
      mechanisms and develop effective vaccines and therapies.
FAU - Cui, Guang-Ying
AU  - Cui GY
AD  - State Key Laboratory for Diagnosis and Treatment of Infectious Disease, First 
      Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, 
      China.
FAU - Diao, Hong-Yan
AU  - Diao HY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Singapore
TA  - Hepatobiliary Pancreat Dis Int
JT  - Hepatobiliary & pancreatic diseases international : HBPD INT
JID - 101151457
RN  - 0 (Hepatitis B Antigens)
SB  - IM
MH  - Acute Disease
MH  - Dendritic Cells/*immunology/*virology
MH  - Hepatitis B Antigens/genetics/*immunology
MH  - Hepatitis B virus/genetics/*immunology
MH  - Hepatitis B, Chronic/genetics/*immunology
MH  - Humans
EDAT- 2010/12/08 06:00
MHDA- 2011/03/26 06:00
CRDT- 2010/12/08 06:00
PHST- 2010/12/08 06:00 [entrez]
PHST- 2010/12/08 06:00 [pubmed]
PHST- 2011/03/26 06:00 [medline]
AID - 1416 [pii]
PST - ppublish
SO  - Hepatobiliary Pancreat Dis Int. 2010 Dec;9(6):584-92.