Mission poorly accomplished: The protective role of natural killer cells in recurrent hepatitis C after liver transplantation

Toll-Like Receptor 3 and 7/8 Function Is Impaired in Hepatitis C Rapid Fibrosis Progression Post-Liver Transplantation

“…NK CD56dim cell IFNγ secretion activates dendritic cells and T cells and promotes anti‐viral Th1 cytokine responses. Impairments in NK cell IFNγ secretion promote Th2 compared with Th1 cytokine responses , leading to impaired activation of T cell immune responses against HCV infection, particularly impairing the protective effect of CD4+ T cells against liver disease progression . Poor immune control of HCV viremia is well described in HCV rapid fibrosis progression and leads to greater proinflammatory cytokine production and greater activation of profibrogenic pathways .…”

Toll‐like receptors in hepatitis C infection: Implications for pathogenesis and treatment

“…Toll-like receptors in hepatitis C infection, and effective CD4+ T-cell responses to HCV are required to mount an active cytotoxic CD8+ T-cell response for viral eradication. [44][45][46][47] T-cell responses to HCV proteins are readily detected early during acute HCV infection, but both CD4+ and CD8+ T-cell function is significantly impaired once chronic infection is established, with reduced cytokine production despite ongoing stimulation with circulating HCV antigens. [48][49][50][51][52][53] One of the key determinants of T-cell function in HCV infection is the quality of antigen presentation by DCs, as this determines the number of epitopes recognized by T cells that will engender an antiviral response.…”

“…The balance between Th1 antiviral and Th2 viral‐permissive T‐cell responses determines viral clearance or persistence, and the degree of inflammation and disease progression . CD4+ T cells have a protective effect against liver disease progression in chronic HCV infection, and effective CD4+ T‐cell responses to HCV are required to mount an active cytotoxic CD8+ T‐cell response for viral eradication . T‐cell responses to HCV proteins are readily detected early during acute HCV infection, but both CD4+ and CD8+ T‐cell function is significantly impaired once chronic infection is established, with reduced cytokine production despite ongoing stimulation with circulating HCV antigens …”