PMID- 18233993
OWN - NLM
STAT- MEDLINE
DCOM- 20080319
LR  - 20080131
IS  - 1352-0504 (Print)
IS  - 1352-0504 (Linking)
VI  - 15
IP  - 3
DP  - 2008 Mar
TI  - Impaired TRAIL-dependent cytotoxicity of CD1c-positive dendritic cells in chronic 
      hepatitis C virus infection.
PG  - 200-11
LID - 10.1111/j.1365-2893.2007.00930.x [doi]
AB  - Dendritic cells (DCs) play a central role in antiviral immunity. Conflicting data 
      on DC function have been reported for hepatitis C virus (HCV) infection. In 
      addition to antigen presentation and cytokine secretion, a subset of human DCs 
      displays direct cytotoxic activity. It has been suggested that measles virus and 
      human immunodeficiency virus (HIV) may enhance cytotoxicity of DCs potentially 
      leading to apoptosis of activated T cells and subsequent down-regulation of 
      antiviral immune responses. We demonstrate that CD1c-positive myeloid DCs, but 
      not BDCA-4-positive plasmacytoid DCs, are able to kill different target cells 
      mainly via tumour necrosis factor-related apoptosis-inducing ligand. The ability 
      of CD1c+ DCs to lyze target cells was found to be completely impaired in patients 
      with chronic hepatitis C (10 chronic HCV patients vs 10 healthy controls; P < 
      0.001) but not in patients with primary biliary cirrhosis. Successful antiviral 
      therapy of chronic hepatitis C rescued the cytotoxicity of DCs. Myeloid DCs of 
      HCV patients and healthy controls had a similar phenotype and endocytotic 
      activity, however, the frequency of mDCs in the peripheral blood was lower (P = 
      0.004) and the allostimulatory function was weaker (P < 0.001) in chronic 
      hepatitis C. Thus, in contrast to HIV and measles virus studies on 
      monocyte-derived DCs, freshly isolated myeloid DCs of patients with hepatitis C 
      do not show an increased but a completely abolished cytotoxic activity. The 
      impaired DC cytotoxicity could represent a novel mechanism for the increased 
      prevalence of autoimmunity in HCV infection.
FAU - Ciesek, S
AU  - Ciesek S
AD  - Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical 
      School, Hannover, Germany.
FAU - Liermann, H
AU  - Liermann H
FAU - Hadem, J
AU  - Hadem J
FAU - Greten, T
AU  - Greten T
FAU - Tillmann, H L
AU  - Tillmann HL
FAU - Cornberg, M
AU  - Cornberg M
FAU - Aslan, N
AU  - Aslan N
FAU - Manns, M P
AU  - Manns MP
FAU - Wedemeyer, H
AU  - Wedemeyer H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Viral Hepat
JT  - Journal of viral hepatitis
JID - 9435672
RN  - 0 (Antigens, CD1)
RN  - 0 (Antigens, Surface)
RN  - 0 (CD1C protein, human)
RN  - 0 (Glycoproteins)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFSF10 protein, human)
RN  - 0 (blood dendritic cell antigen 4, human)
SB  - IM
MH  - Adult
MH  - Antigens, CD1/analysis
MH  - Antigens, Surface/analysis
MH  - Apoptosis
MH  - Cells, Cultured
MH  - Cytotoxicity Tests, Immunologic
MH  - *Cytotoxicity, Immunologic
MH  - Dendritic Cells/chemistry/*immunology
MH  - Female
MH  - Glycoproteins/analysis
MH  - Hepatitis C, Chronic/drug therapy/*immunology
MH  - Humans
MH  - Liver Cirrhosis, Biliary/immunology
MH  - Male
MH  - Middle Aged
MH  - TNF-Related Apoptosis-Inducing Ligand/*physiology
EDAT- 2008/02/01 09:00
MHDA- 2008/03/20 09:00
CRDT- 2008/02/01 09:00
PHST- 2008/02/01 09:00 [pubmed]
PHST- 2008/03/20 09:00 [medline]
PHST- 2008/02/01 09:00 [entrez]
AID - JVH930 [pii]
AID - 10.1111/j.1365-2893.2007.00930.x [doi]
PST - ppublish
SO  - J Viral Hepat. 2008 Mar;15(3):200-11. doi: 10.1111/j.1365-2893.2007.00930.x.