Chronic Hepatitis C Pathogenesis: Immune Response in the Liver Microenvironment and Peripheral Compartment

Chronic hepatitis C (CHC) pathogenic mechanisms as well the participation of immune response in generation liver damage are still a topic interest. Here, we evaluated cell populations and cytokines peripheral blood (PB) to elucidate their role CHC pathogenesis. B, CTL, Th, Treg, Th1, Th17, NK localization frequency were on biopsies by immunohistochemistry, while frequency, differentiation, functional status PB flow cytometry. TNF-α, IL-23, IFN- γ , IL-1β, IL-6, IL-8, IL-17A, IL-21, IL-10, TGF-β expression levels quantified fresh biopsy RT-qPCR plasma CBA/ELISA. Liver CTL Th1 at lobular area inversely correlated with viral load (r = −0.469, p =0.003 r −0.384, 0.040). Treg 0.784, < 0.0001; 0.436, 0.013). Th17 hepatic IL-8 0.52, 0.05), both higher advanced fibrosis cases (Th17 0.0312, 0.009). Hepatic severe (IL-1β 0.026, IL-23 0.031, 0.002, TGF-β, 0.037). Peripheral ( 0.008) dim 0.018) diminished, bright 0.025) was elevated patients vs. donors. Naïve Th 0.011) 0.0007) decreased, activated 0.0003) increased. production degranulation activity normal. showed an altered profile donors, particularly IL-6 0.041). Total CTLs favored damage. could not prevent fibrogenesis triggered IL-8. T-lymphocyte differentiation stage shift, cytokine NK-cell count decrease would contribute global disease.