title: Elevated IL-6 receptor expression on CD4+ T cells contributes to the increased Th17 responses in patients with chronic hepatitis B.
abstract: BACKGROUND
  Increased 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).
  
  
  METHODS
  Th17 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.
  
  
  RESULTS
  All 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.
  
  
  CONCLUSIONS
  we showed that enhancement of IL-6R expression on CD4+ T cells upon HBV infection contributes to increased Th17 response in patients with CHB.
authors.affiliation: Department of Infectious Diseases, the third affiliated hospital of Sun-Yat-Sen university, Guangzhou, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Zhang
authors.forename: Simin
authors.initials: S
authors.lastname: Yao
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Mingxia
authors.initials: M
authors.lastname: Zhang
authors.forename: Qing
authors.initials: Q
authors.lastname: He
authors.forename: Guilin
authors.initials: G
authors.lastname: Yang
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Gao
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.forename: Xinchun
authors.initials: X
authors.lastname: Chen
authors.forename: Boping
authors.initials: B
authors.lastname: Zhou
mesh_terms: D000293:Adolescent; D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology*; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression; D020869:Gene Expression Profiling; D006515:Hepatitis B virus / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000276:immunology*; D006801:Humans; D020381:Interleukin-17 / Q000378:metabolism*; D008297:Male; D019947:Receptors, Interleukin-6 / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050378:T-Lymphocytes, Regulatory / Q000737:chemistry / Q000276:immunology*; D058504:Th17 Cells / Q000737:chemistry / Q000276:immunology*; D055815:Young Adult
chemical_list: D020381:Interleukin-17; D019947:Receptors, Interleukin-6