title: Enhanced peripheral γδT cells cytotoxicity potential in patients with HBV-associated acute-on-chronic liver failure might contribute to the disease progression.
abstract: BACKGROUND
  The current study explored the characteristics of γδ T cells in the blood of HBV-associated acute-on-chronic liver failure (HBV-ACLF) patients and examined the relationship between γδ T cells and the clinical parameters.
  
  
  METHODS
  Blood samples were obtained from 26 patients with HBV-ACLF, 40 patients with chronic hepatitis B virus (HBV) infection (CHBV), and 25 healthy controls (HC). The frequencies of γδ T cells, subtype Vδ1T or Vδ2T, and CD45RO(+)γδ T cells were determined using flow cytometry. Intracellular cytokine staining analysis was used to evaluate the proportion of the IFN-γ-, TNF-α-, or IL-17-producing γδ T cells, and CD107a- or granzyme B-positive γδ T cells.
  
  
  RESULTS
  We found that the proportion of γδ T cells in blood samples from HBV-ACLF patients was much lower than in samples from CHBV patients or healthy controls. After stimulation with PMA and ionomycin, γδ T cells from HBV-ACLF patients produced the greatest amount of TNF-α or IL-17 among the three groups. Granzyme B- or CD107a-positive γδ T cells were significantly more frequent than in CHBV or control samples. There was a negative correlation between the percent of TNF-α(+)γδ T cells and ALT or AST levels, and between the percent of CD107a(+)γδ T cells and TBiL or DBiL levels.
  
  
  CONCLUSIONS
  These results suggest that γδ T cells might participate in liver injury in HBV-ACLF patients by producing increased amounts of inflammatory cytokines and/or cytotoxicity ability. These findings provide novel information regarding the pathogenesis of HBV-ACLF.
authors.affiliation: Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Institute for Viral Hepatitis, Department of Infectious Diseases, Second Affiliated Hospital, Chongqing Medical University, No.74 Lin Jiang Rd., Yu Zhong District, 400010, Chongqing, People's Republic of China. chenggming@yahoo.com.cn
authors.forename: Min
authors.initials: M
authors.lastname: Chen
authors.forename: Peng
authors.initials: P
authors.lastname: Hu
authors.forename: Hui
authors.initials: H
authors.lastname: Peng
authors.forename: Weiqun
authors.initials: W
authors.lastname: Zeng
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Shi
authors.forename: Yu
authors.initials: Y
authors.lastname: Lei
authors.forename: Huaidong
authors.initials: H
authors.lastname: Hu
authors.forename: Dazhi
authors.initials: D
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Ren
mesh_terms: D000328:Adult; D000368:Aged; D003602:Cytotoxicity, Immunologic; D018450:Disease Progression; D058625:End Stage Liver Disease / Q000276:immunology* / Q000821:virology; D005260:Female; D053804:Granzymes / Q000378:metabolism; D006509:Hepatitis B / Q000150:complications / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000096:biosynthesis; D015759:Ionomycin / Q000494:pharmacology; D017114:Liver Failure, Acute / Q000276:immunology* / Q000821:virology; D052118:Lysosomal-Associated Membrane Protein 1 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult
chemical_list: D020381:Interleukin-17; D052118:Lysosomal-Associated Membrane Protein 1; D016692:Receptors, Antigen, T-Cell, gamma-delta; D014409:Tumor Necrosis Factor-alpha; D015759:Ionomycin; D007371:Interferon-gamma; D053804:Granzymes