期刊
CLINICAL IMMUNOLOGY
卷 117, 期 1, 页码 57-64出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2005.06.003
关键词
chronic hepatitis C; T-cells; Th1/Th2 profile; IL-10; IFN-gamma; immunotherapy; cytokines
类别
Chronic hepatitis C virus (HCV) infection is associated with weak CD4+ T-helper type I 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 I antiviral T-cell reactivity with an increased frequency of liCV-specific IFN-gamma producing T-cells and IFN-gamma 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. (c) 2005 Elsevier Inc. All rights reserved.
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