Abstract
BackgroundIncreased numbers of Interleukin-17-producing CD4+ T cells (Th17) have been found in association with hepatitis B virus (HBV)-induced liver injury. However, the mechanism underlying the increase of Th17 responses in patients with HBV infection remains unclear. In this study, we investigate the possible regulatory mechanisms of increased Th17 responses in patients with chronic hepatitis B(CHB).MethodsTh17 response and IL-6R expression on CD4+ T cells in peripheral blood samples were determined by flow cytometry. Cytokines TGF-β, IL-1β, IL-6 and IL-17 in plasma and/or supernatant samples were determined by ELISA and the IL-17 and IL-6R mRNA levels were quantified by quantitative real-time reverse polymerase chain reaction.ResultsAll these data indicated that the frequency of periphery Th17 cells is significantly correlated with the percentage of CD4+ T cells expressing IL-6R in CHB patients. CD4+ T cells from patients with CHB, but not those from healthy donors, produced higher levels of IL-17 and had more IL-6R expression upon stimulation with the HBV core antigen (HBcAg) in vitro. The PMA/ionomycin and HBcAg -stimulated up-regulation of IL-17 production by CD4+ T cells could be reversed by a neutralizing antibody against IL-6R.Conclusionwe showed that enhancement of IL-6R expression on CD4+ T cells upon HBV infection contributes to increased Th17 response in patients with CHB.
Highlights
Increased numbers of Interleukin-17-producing CD4+ T cells (Th17) have been found in association with hepatitis B virus (HBV)-induced liver injury
Increased Th17 responses were associated with liver injury in patients with HBV infection Previous studies within chronic hepatitis B (CHB) patients suggested that Th17 cells play an important role in HBV-induced inflammatory responses [17,18,19,20]
To better understand the role of Th17 cells in HBV infection, we extended these findings by comparing Th17 responses in patients with acute hepatitis B (AHB), asymptomatic HBV carrier (AsC), as well as patients with CHB
Summary
Increased numbers of Interleukin-17-producing CD4+ T cells (Th17) have been found in association with hepatitis B virus (HBV)-induced liver injury. The mechanism underlying the increase of Th17 responses in patients with HBV infection remains unclear. We investigate the possible regulatory mechanisms of increased Th17 responses in patients with chronic hepatitis B(CHB). Zhang et al reported that antigen non-specific Th17 response was increased in patients with chronic hepatitis B (CHB) and the peripheral Th17 frequency in CHB patients was closely associated with the degree of liver damage which determined by serum alanine amino-transferase (ALT) levels and liver histological activity index(HAI) scores [17]. The regulatory mechanism of Th17 responses in patients with HBV infection remains unclear
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