Approximately 70% of patients infected with hepatitis C virus (HCV) develop chronic infection, which has been reported to be due to impaired specific T cell responses. Myeloid dendritic cells (mDCs) are potent antigen-presenting cells that regulate T cell responses, however their role during chronic hepatitis C (CHC) is not fully understood. My hypothesis was that the activity of mDCs to regulate T-cell response against HCV might be changed during CHC infection, and this change might contribute to the impaired T-cell responses that lead to the persistence of HCV infection. The objectives of my thesis were to compare the immunogenic activity (which stimulates T-cell proliferation), tolerogenic activity (which kills T cells), and apoptosis of mDCs from CHC patients and healthy donors. In this thesis, I found that mDCs from CHC patients expressed lower level of activating molecules, HLA-DR and CD86, compared to mDCs from healthy volunteers. When mDCs were cocultured with T cells, there were fewer T cells proliferating in the patient group than in the healthy group. This result indicated that the ability of mDCs to stimulate T cell proliferation was impaired in CHC patients. Moreover, mDCs from CHC patients underwent spontaneous apoptosis at a higher rate than mDCs from healthy donors. Nuclear factor-kappa B (NF-κB) activity, which is critical for mDC function and prevention of apoptosis, was diminished in mDCs from CHC patients. I further studied the tolerogenic activity of mDCs during CHC infection. mDCs from CHC patients expressed up-regulated levels of Fas ligand and the ligand 2 of PD-1 compared to mDCs from healthy volunteers. mDCs from CHC patients can kill T cells, while mDCs from healthy volunteers could not. This result indicated that the tolerogenic activity of mDCs was up-regulated in CHC patients. In conclusion, mDCs from CHC patients demonstrated functional changes with increased apoptosis, and diminished NF-κB activity. mDCs from CHC patients have impaired immunogenic activity to stimulate T-cell proliferation, and have up-regulated tolerogenic activity to kill T cells. These changes might be additional novel mechanisms of immune evasion by HCV, and contribute to the impaired specific T-cell responses observed in CHC patients.