title: High levels of FCγR3A and PRF1 expression in peripheral blood mononuclear cells from patients with primary biliary cirrhosis.
abstract: BACKGROUND
  Innate immunity plays an important role in the pathogenesis of primary biliary cirrhosis (PBC) that needs to be characterized. Levels and clinical relationship of Fc gamma receptor III-A (FcγR3A), tyrosine kinase binding protein (TYROBP) and perforin-1 (PRF1), important genes for nature killer (NK) cells, were analyzed in PBC patients.
  
  
  OBJECTIVE
  The purpose of this study was to explore the expression levels of the above-mentioned genes in peripheral blood mononuclear cells (PBMCs) from PBC patients.
  
  
  METHODS
  A total of 102 PBC patients and 85 healthy controls (HC) were recruited. The relative levels of FCγR3A, TYROBP, and PRF1 mRNA transcripts in PBMCs were determined by RT-PCR. The percentages of peripheral blood NK, natural killer T (NKT), FCγR3A(+) or PRF1(+) NK cells and PRF1(+) NKT cells in PBC patients and HC were also characterized by flow cytometry analysis. The potential associations of the percentages of NK and NKT cells with clinical indexes were analyzed.
  
  
  RESULTS
  The relative levels of FCγR3A, TYROBP, and PRF1 mRNA transcripts and the percentages of PRF1(+) NK and NKT cells in PBC patients were significantly higher than that in HC. Moreover, the percentages of PRF1-expressing NK and NKT cells in PBC patients were negatively associated with the levels of serum gamma-glutamyltransferase (GGT) and Mayo risk scores, and the relative levels of FCγR3A expression in NK cells of PBC patients were positively associated with the levels of serum GGT.
  
  
  CONCLUSIONS
  FCγR3A and PRF1 may participate in the pathogenesis and progression of PBC.
authors.affiliation: Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, No. 41 Da Mu Cang, Western District, Beijing, 100032, People's Republic of China. lis8858@163.com
authors.forename: Shan
authors.initials: S
authors.lastname: Li
authors.forename: Danxu
authors.initials: D
authors.lastname: Ma
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Xi
authors.initials: X
authors.lastname: Li
authors.forename: Chuiwen
authors.initials: C
authors.lastname: Deng
authors.forename: Xue
authors.initials: X
authors.lastname: Qin
authors.forename: Ting
authors.initials: T
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.forename: Qun
authors.initials: Q
authors.lastname: Shi
authors.forename: Qian
authors.initials: Q
authors.lastname: Wang
authors.forename: Qingjun
authors.initials: Q
authors.lastname: Wu
authors.forename: Xuan
authors.initials: X
authors.lastname: Zhang
authors.forename: Fengchun
authors.initials: F
authors.lastname: Zhang
authors.forename: Yongzhe
authors.initials: Y
authors.lastname: Li
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics; D000328:Adult; D000368:Aged; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics* / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D008105:Liver Cirrhosis, Biliary / Q000235:genetics / Q000276:immunology*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D008875:Middle Aged; D055611:Natural Killer T-Cells / Q000276:immunology*; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins / Q000235:genetics*; D017452:Receptors, IgG / Q000235:genetics*; D012720:Severity of Illness Index
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C496124:FCGR3A protein, human; D008565:Membrane Proteins; C510468:PRF1 protein, human; D052899:Pore Forming Cytotoxic Proteins; D017452:Receptors, IgG; C110546:TYROBP protein, human; D054353:Perforin