Blocking of interleukin-10 receptor - A novel approach to stimulate T-helper cell type 1 responses to hepatitis C virus
dc.creator | Rigopoulou, E. I. | en |
dc.creator | Abbott, W. G. H. | en |
dc.creator | Haigh, P. | en |
dc.creator | Naoumov, N. V. | en |
dc.date.accessioned | 2015-11-23T10:46:25Z | |
dc.date.available | 2015-11-23T10:46:25Z | |
dc.date.issued | 2005 | |
dc.identifier | 10.1016/j.clim.2005.06.003 | |
dc.identifier.issn | 15216616 | |
dc.identifier.uri | http://hdl.handle.net/11615/32625 | |
dc.description.abstract | Chronic hepatitis C virus (HCV) infection is associated with weak CD4+ T-helper type 1 reactivity and enhanced interleukin-10 production to HCV antigens. Here we demonstrate in vitro that monoclonal antibody-induced blockade of IL-10 receptor (IL-10R) generates a favorable balance of CD4+ T-cell responses to HCV. The addition of anti-IL-10R to mononuclear cells leads to a dose-dependent increase of T-cell proliferative response to HCV core, non-structural proteins 3 and 4. In competition experiments, anti-IL-10R reversed the inhibitory effect of IL-10 on HCV-specific T-cell proliferation. Furthermore, the blockade of IL-10R altered the balance towards type 1 antiviral T-cell reactivity with an increased frequency of HCV-specific IFN-γ producing T-cells and IFN-γ secretion. The impact of IL-10R blockade on T-cell reactivity to HCV demonstrates the major role of IL-10 in suppressing antiviral T-cell responses. Blocking IL-10 activity may be a useful immunotherapy approach to enhance the efficacy of antiviral treatment in chronic hepatitis C. © 2005 Elsevier Inc. All rights reserved. | en |
dc.source.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-27244444359&partnerID=40&md5=65fd778f3074d13c6774227e1c7e02ff | |
dc.subject | Chronic hepatitis C | en |
dc.subject | Cytokines | en |
dc.subject | IFN-γ | en |
dc.subject | IL-10 | en |
dc.subject | Immunotherapy | en |
dc.subject | T-cells | en |
dc.subject | Th1/Th2 profile | en |
dc.subject | CD4 antigen | en |
dc.subject | core protein | en |
dc.subject | gamma interferon | en |
dc.subject | hepatitis C antigen | en |
dc.subject | interleukin 10 | en |
dc.subject | interleukin 10 receptor | en |
dc.subject | interleukin 10 receptor antibody | en |
dc.subject | monoclonal antibody | en |
dc.subject | monoclonal antibody 3c5 2 | en |
dc.subject | monoclonal antibody 3F9 | en |
dc.subject | non structural protein 4 | en |
dc.subject | nonstructural protein 3 | en |
dc.subject | receptor antibody | en |
dc.subject | unclassified drug | en |
dc.subject | interleukin receptor | en |
dc.subject | adult | en |
dc.subject | antigen antibody reaction | en |
dc.subject | article | en |
dc.subject | cell specificity | en |
dc.subject | cellular immunity | en |
dc.subject | competitive inhibition | en |
dc.subject | concentration response | en |
dc.subject | controlled study | en |
dc.subject | cytokine production | en |
dc.subject | cytokine release | en |
dc.subject | female | en |
dc.subject | hepatitis C | en |
dc.subject | Hepatitis C virus | en |
dc.subject | human | en |
dc.subject | human cell | en |
dc.subject | immunoreactivity | en |
dc.subject | immunostimulation | en |
dc.subject | in vitro study | en |
dc.subject | lymphocyte proliferation | en |
dc.subject | male | en |
dc.subject | priority journal | en |
dc.subject | receptor blocking | en |
dc.subject | T lymphocyte | en |
dc.subject | Th1 cell | en |
dc.subject | virus core | en |
dc.subject | virus immunity | en |
dc.subject | biosynthesis | en |
dc.subject | cell proliferation | en |
dc.subject | comparative study | en |
dc.subject | drug antagonism | en |
dc.subject | drug effect | en |
dc.subject | immunology | en |
dc.subject | middle aged | en |
dc.subject | virology | en |
dc.subject | Antibodies, Monoclonal | en |
dc.subject | Hepacivirus | en |
dc.subject | Humans | en |
dc.subject | Interferon Type II | en |
dc.subject | Interleukin-10 | en |
dc.subject | Receptors, Interleukin | en |
dc.subject | Receptors, Interleukin-10 | en |
dc.subject | Th1 Cells | en |
dc.title | Blocking of interleukin-10 receptor - A novel approach to stimulate T-helper cell type 1 responses to hepatitis C virus | en |
dc.type | journalArticle | en |
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