Immune response of Th17‐associated cytokines by peripheral blood mononuclear cells from patients with chronic hepatitis C virus infection
HighlightsChronic HCV infection caused immune dysregulation.Th17 cells and their associated cytokines were involved in this process.HCV core and NS3 antigens induced Th17 immune responses in patients. Abstract Hepatitis C virus (HCV) chronic infection causes severe cellular immune dysfunction. Here, we investigated the production of Th17‐associated cytokines by peripheral blood mononuclear cells (PBMCs) of untreated patients with HCV, patients presenting an early virologic response (EVR) after 12 weeks of treatment with interferon‐&agr; plus ribavirin with or without HCV protease inhibitors, and patients who were nonresponders to HCV therapy. PBMCs were stimulated with HCV core and nonstructural antigens, and the production of Th17‐associated cytokines was measured with a Milliplex MAP immunoassay. Core‐stimulated PBMCs from both untreated and nonresponder patients produced interleukin (IL)‐17A, and vigorous production of IL‐17A in response to NS3 antigen was only verified in the untreated group. Nonresponder patients also produced IL‐17F after core antigen stimulation. IL‐21 production was unaltered in the three groups of patients, whereas IL‐17E and IL‐22 were not detected. The production of Th17 cytokines by cells from patients showing an EVR was insignificant. IL‐17A and IL‐17F levels were not correlated with alanine aminotransferase levels or viremia. However, advanced fibrosis was associated with higher IL‐17A production in T0 cells stimulated with core antigen. Untreated patients with HCV and patients who were nonresponders to antiviral treatment differed in their PBMC immune responses of Th17‐associated cytokines. The early virological response to antiviral treatment dramatically decreased Th17 immune responses to HCV antigens.