title: Decreased Vδ2 γδ T cells associated with liver damage by regulation of Th17 response in patients with chronic hepatitis B.
abstract: BACKGROUND
  γδ T cells comprise a small subset of T cells and play a protective role against cancer and viral infections; however, their precise role in patients with chronic hepatitis B remains unclear.
  
  
  METHODS
  Flow cytometry and immunofunctional assays were performed to analyze the impact of Vδ2 γδ (Vδ2) T cells in 64 immune-activated patients, 22 immune-tolerant carriers, and 30 healthy controls.
  
  
  RESULTS
  The frequencies of peripheral and hepatic Vδ2 T cells decreased with disease progression from immune tolerant to immune activated. In the latter group of patients, the decreases in peripheral and intrahepatic frequencies of Vδ2 T cells reversely correlated with alanine aminotransferase levels and histological activity index. These activated terminally differentiated memory phenotypic Vδ2 T cells exhibited impaired abilities in proliferation and chemotaxis, while maintained a relative intact interferon (IFN) γ production. Importantly, Vδ2 T cells, in vitro, significantly suppressed the production of cytokines associated with interleukin 17-producing CD4+ T (Th17) cells through both cell contact-dependent and IFN-γ-dependent mechanisms.
  
  
  CONCLUSIONS
  Inflammatory microenvironment in IA patients result in decreased numbers of Vδ2 T cells, which play a novel role by regulating the pathogenic Th17 response to protect the liver in patients with chronic hepatitis B.
authors.affiliation: State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Wu
authors.forename: Ji-Yuan
authors.initials: JY
authors.lastname: Zhang
authors.forename: Ang
authors.initials: A
authors.lastname: Huang
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Li
authors.forename: Song
authors.initials: S
authors.lastname: Zhang
authors.forename: Jun
authors.initials: J
authors.lastname: Wei
authors.forename: Siyuan
authors.initials: S
authors.lastname: Xia
authors.forename: Yajuan
authors.initials: Y
authors.lastname: Wan
authors.forename: Weiwei
authors.initials: W
authors.lastname: Chen
authors.forename: Zheng
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yangguang
authors.initials: Y
authors.lastname: Li
authors.forename: Ti
authors.initials: T
authors.lastname: Wen
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Youjia
authors.initials: Y
authors.lastname: Cao
authors.forename: Puyue
authors.initials: P
authors.lastname: Wang
authors.forename: Liqing
authors.initials: L
authors.lastname: Zhao
authors.forename: Zhenzhou
authors.initials: Z
authors.lastname: Wu
authors.forename: Fu-Sheng
authors.initials: FS
authors.lastname: Wang
authors.forename: Zhinan
authors.initials: Z
authors.lastname: Yin
mesh_terms: D000293:Adolescent; D000328:Adult; D048708:Cell Growth Processes / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D016207:Cytokines / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D019694:Hepatitis B, Chronic / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology*; D018709:Statistics, Nonparametric; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D016692:Receptors, Antigen, T-Cell, gamma-delta