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AIM:Cytokine release by macrophages critically determinesthe type of immune response to an antigen.Therefore,westudied hepatitis C virus(HCV)-specific induction ofinterleukins-1β,-10,-12(IL-1β,IL-10,IL-12),and tumornecrosis factor-α(TNF-α)in monocytes.METHODS:Intracallular cytokine expression was studied byflow cytometry in 23 patients with chronic hepatitis C,14anti-HCV seropositives without viremia and 11 controls afterstimulation of peripheral blood mononuclear calls withrecombinant core,NS3,NS4,NSSa and NSSb proteins.RESULTS:Patients with HCV viremia revealed greaterspontaneous expression of IL-1β,TNF-α,and IL-10.Furthermore,greater than twofold higher IL-10 expressionwas induced by the HCV antigens in chronic hepatitis C thanin the other two groups(P<0.05).In contrast,neither IL-12 nor TNF-α was induced preferentially.CONCLUSION:In chronic hepatitis C antigen-specificcytokine induction in monocytes is apparently shiftedtowards predominant IL-10 induction-not counterbalancedby antiviral type 1 cytokines.This may contribute topersistent viral replication.
AIM: Cytokine release by macrophages critically determine type of immune response to an antigen. Before, Westudied hepatitis C virus (HCV) -specific induction of interleukins-1β, -10, -12 (IL-1β, IL-10, IL- 12) , and tumornecrosis factor-α (TNF-α) in monocytes. METHODS: Intracallular cytokine expression was studied by flow cytometry in 23 patients with chronic hepatitis C, 14anti-HCV seropositives without viremia and 11 controls afterstimulation of peripheral blood mononuclear calls withrecombinant core, NS3 , NS4, NSSa and NSSb proteins .RESULTS: Patients with HCV viremia revealed greaterspontaneous expression of IL-1β, TNF-α, and IL-10.Furthermore, greater than twofold higher IL-10 expressionwas induced by the HCV antigens in chronic hepatitis C In contrast, neither IL-12 nor TNF-αwas induced preferentially. CONCLUSION: In chronic hepatitis C antigen-specificcytokine induction in monocytes is apparently shiftedtowards predominant IL-10 induction-not counterbalanced by antiviral type 1 cytokines.This may contribute topersistent viral replication.