TY - JOUR
T1 - The affect of chronic hepatitis C infection on dendritic cell function
T2 - A summary of the experimental evidence
AU - Ryan, E. J.
AU - O'Farrelly, C.
N1 - © 2011 Blackwell Publishing Ltd.
PY - 2011/9
Y1 - 2011/9
N2 - Chronic hepatitis C virus (HCV) infection occurs in patients who fail to mount an effective T-cell response against the virus. One hypothesis for poor anti-viral immunity in these patients is that the virus impedes the immune response by disabling dendritic cells (DCs), cells that play a key role in pathogen recognition and initiation of adaptive immunity. Initial studies in the 1990s supported this hypothesis, as they clearly demonstrated that monocyte-derived DCs obtained from patients with chronic HCV infection displayed a reduced ability to stimulate lymphocyte proliferation. However, over the last 20 years, the situation has become more ambiguous. Many studies support the initial observation of a DC defect, while others using different patient cohorts or technologies have clearly demonstrated intact DC function in patients with chronic HCV. It is likely that the true situation lies somewhere in between. Just as there is a spectrum of disease in patients with chronic HCV, DCs obtained from different patients may display different properties. It is important to reconcile these divergent findings, as a clearer understanding of how the virus affects DC function will facilitate the development of immunotherapy and therapeutic vaccination strategies for patients with chronic HCV infection.
AB - Chronic hepatitis C virus (HCV) infection occurs in patients who fail to mount an effective T-cell response against the virus. One hypothesis for poor anti-viral immunity in these patients is that the virus impedes the immune response by disabling dendritic cells (DCs), cells that play a key role in pathogen recognition and initiation of adaptive immunity. Initial studies in the 1990s supported this hypothesis, as they clearly demonstrated that monocyte-derived DCs obtained from patients with chronic HCV infection displayed a reduced ability to stimulate lymphocyte proliferation. However, over the last 20 years, the situation has become more ambiguous. Many studies support the initial observation of a DC defect, while others using different patient cohorts or technologies have clearly demonstrated intact DC function in patients with chronic HCV. It is likely that the true situation lies somewhere in between. Just as there is a spectrum of disease in patients with chronic HCV, DCs obtained from different patients may display different properties. It is important to reconcile these divergent findings, as a clearer understanding of how the virus affects DC function will facilitate the development of immunotherapy and therapeutic vaccination strategies for patients with chronic HCV infection.
KW - cellular immune response
KW - cytokines
KW - dendritic cell
KW - hepatitis C Virus
KW - immune evasion
UR - http://www.scopus.com/inward/record.url?scp=79960959972&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2893.2011.01453.x
DO - 10.1111/j.1365-2893.2011.01453.x
M3 - Review article
C2 - 21794024
AN - SCOPUS:79960959972
SN - 1352-0504
VL - 18
SP - 601
EP - 607
JO - Journal of Viral Hepatitis
JF - Journal of Viral Hepatitis
IS - 9
ER -