Immune dysregulations in patients with chronic hepatitis C are still poorly understood, particularly their inflammatory pathways. Recent studies have shown that transforming growth factor β (TGF-β) alone promotes the generation of anti-inflammatory regulatory T lymphocytes (T-reg) from nal¨ve T CD4+ cells, while TGF-β in concert with interleukin 6 (IL-6) promotes Th17 cells that produce IL-17. We studied serum levels of IL-17 and its known activators (IL-6, TGF-β) in 55 hepatitis C patients and 33 age- and gender-matched healthy subjects. Cytokine levels were quantified by sandwich enzyme-linked immunosorbent assays. Surprisingly, IL-17 serum levels were significantly higher in healthy subjects than in hepatitis C patients (16.5 ±6.6 pg/ml vs. 8.1 ±5.5 pg/ml; p < 0.0000). By contrast, serum
TGF-β levels were significantly lower in healthy subjects (30.9 ±7.4 ng/ml vs. 40.7 ±20.6 ng/ml; p = 0.0327). Serum levels of IL-6 did not differ between groups but correlated positively with the stage of fibrosis in hepatitis C patients (r = 0.36; p = 0.005). Our findings suggest that hepatitis C virus down-regulates IL-17 production and up-regulates TGF-β production. The increased level of TGF-β in HCV patients may be responsible for suppressing IL-17 production by Th17 cells.