PMID- 22853328
OWN - NLM
STAT- MEDLINE
DCOM- 20130211
LR  - 20220321
IS  - 1348-0421 (Electronic)
IS  - 0385-5600 (Linking)
VI  - 56
IP  - 10
DP  - 2012 Oct
TI  - Hepatitis B virus surface antigen can activate human monocyte-derived dendritic 
      cells by nuclear factor kappa B and p38 mitogen-activated protein kinase mediated 
      signaling.
PG  - 719-27
LID - 10.1111/j.1348-0421.2012.00496.x [doi]
AB  - Hepatitis B virus Ag (HBsAg), a major antigen of hepatitis B virus (HBV), is also 
      a vaccine component for prevention of HBV infection. Dendritic cells (DCs) of HBV 
      carriers reportedly exhibit functional impairment. In this study, the aim was to 
      investigate the effect of HBsAg on activation of human monocyte-derived dendritic 
      cells (MD-DCs), and the subsequent signal transduction pathway. Treatment of 
      MD-DCs with HBsAg resulted in enhanced cell surface expression of cluster of 
      differentiation 80, CD83, CD86 and major histocompatibility complex class II, and 
      increased interleukin (IL)-12 p40, IL-12p70, and IL-10 production. Furthermore, 
      HBsAg treatment of MD-DCs with HBsAg resulted in enhanced T cell-stimulatory 
      capacity and increased T cell secretion of interferon and IL-10. The pathway of 
      MD-DCs activation by HBsAg was further investigated in the present study. 
      Inhibition of nuclear factor (NF)-kappa B (kappaB) by helenalin and p38 
      mitogen-activated protein kinase (MAPK) by SB203580 prevented production of IL-12 
      p40, IL-12 p70, and IL-10. HBsAg also augmented MAPK phosphorylation. Thus, 
      cytokine secretion of human MD-DCs by HBsAg is blocked by inhibition of the NF-kappaB 
      and p38 MAPK pathways. Likewise, decreased inhibition of kappa B alpha 
      concentrations and MAPK phosphorylation are critical for MD-DC maturation by 
      HBsAg. These findings may provide a strategy for improving the prophylactic and 
      therapeutic efficacy of vaccines and tumor therapies that utilize these pathways.
CI  - (c) 2012 The Societies and Wiley Publishing Asia Pty Ltd.
FAU - Jan, Rong-Hwa
AU  - Jan RH
AD  - Institute of Medical Sciences, Tzu-Chi University, National Taiwan University 
      Hospital, Taipei, Taiwan.
FAU - Lin, Yu-Li
AU  - Lin YL
FAU - Chen, Chia-Jung
AU  - Chen CJ
FAU - Lin, Teng-Yi
AU  - Lin TY
FAU - Hsu, Ya-Chun
AU  - Hsu YC
FAU - Chen, Li-Kuang
AU  - Chen LK
FAU - Chiang, Bor-Luen
AU  - Chiang BL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Microbiol Immunol
JT  - Microbiology and immunology
JID - 7703966
RN  - 0 (Antigens, CD)
RN  - 0 (Hepatitis B Surface Antigens)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Interleukins)
RN  - 0 (NF-kappa B)
RN  - 9008-11-1 (Interferons)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Antigens, CD/analysis
MH  - Cells, Cultured
MH  - Dendritic Cells/chemistry/*immunology
MH  - Hepatitis B Surface Antigens/*immunology
MH  - Histocompatibility Antigens Class II/analysis
MH  - Humans
MH  - Interferons/metabolism
MH  - Interleukins/metabolism
MH  - NF-kappa B/*metabolism
MH  - *Signal Transduction
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2012/08/03 06:00
MHDA- 2013/02/12 06:00
CRDT- 2012/08/03 06:00
PHST- 2012/08/03 06:00 [entrez]
PHST- 2012/08/03 06:00 [pubmed]
PHST- 2013/02/12 06:00 [medline]
AID - 10.1111/j.1348-0421.2012.00496.x [doi]
PST - ppublish
SO  - Microbiol Immunol. 2012 Oct;56(10):719-27. doi: 10.1111/j.1348-0421.2012.00496.x.