| Summary: | 碩士 === 國立成功大學 === 醫學檢驗生物技術學系 === 94 === Hepatitis C virus (HCV) diseases threaten global human health. The current treatment for chronic HCV infection with combination regimen of pegylated interferon (IFN)-alpha and ribavirin can exert overall response rate of approximately 46-78%, which is influenced by viral genotype, initial circulating viral load and host factors. Host factors such as immunological regulators seem to affect the outcome of antiviral treatment of pegylated IFN-alpha and ribavirin since both agents are known immumodulators. Proper antigen presentation function is required to elicit sufficient adapted cellular immunity against viral infection, which has been impaired in patients chronically infected with HCV. This study aims to investigate whether the modulation of immuno-surface proteins by pegylated interferon (IFN)-alpha and ribavirin is related to therapeutic responses. We enrolled 35 patients with chronic hepatitis C, who have undergone combination therapy. We longitudinally assessed the effect of anti-HCV agents on the expression levels of CD81, HLA-ABC, CD86 and CD28, the three major components in trigger of antigen-dependent and antigen-independent co-stimulatory signals, in peripheral blood mononuclear cells (PBMCs) from patients receiving combination therapy for 24 weeks and afterward follow-up for 24 weeks. FACS analysis showed that HLA-ABC and CD86 upregulation on B cells during combine therapy in patients with sustained virological response (SVR) (n=26), but not in patients without SVR (n=9). Elevation of surface HLA-ABC expression was not secondary to increased RNA levels in B cells. The treatment induced upregulation of surface CD28 in CD4+ and CD8+ T cells in both of the patient groups. The analysis of polymorphic HLA-ABC alleles showed no significant difference in both patient groups. In conclusion, the expression levels of HLA-ABC and CD86 were up-regulated on B cells during combination therapy only in patients with SVR but not non-SVR.
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