title: [Expression and significance of Tim-3 on peripheral blood monocytes in patients with chronic hepatitis B].
abstract: OBJECTIVE
  To detect T cell immunoglobulin and mucin domain-containing molecule 3(Tim-3) expression on peripheral blood monocyts (PBMs) and explore its effect on inflammatory cytokines production of PBMs in patients with chronic hepatitis B (CHB).
  
  
  METHODS
  The expression of Tim-3 protein and mRNA on PBM subsets was respectively determined using flow cytometry and real-time quantitative RT-PCR (qRT-PCR) in CHB patients at different phases. After PBMs were stimulated with both recombinant human galectin-9 and lipopolysaccharide (LPS) in active CHB patients, the supernatants were collected to measure the levels of proinflammatory factors including TNF-α, IL-1β and IL-6 by ELISA.
  
  
  RESULTS
  Compared with healthy controls and CHB patients at immune active (IA) phase, the expression of Tim-3 was significantly up-regulated in PBMs of CHB patients at immune tolerance (IT) phase (P<0.01). The level of Tim-3 expression on both CD14(+);CD16-; and CD14(+);CD16(+); monocyte subsets of CHB patients at IT phase was significantly higher than that of the CHB patients at IA phase and of healthy controls (P<0.05). qRT-PCR further demonstrated that the level of Tim-3 mRNA on monocytes of CHB patients at IA phase was also higher than that of healthy controls (P=0.040). There was a positive correlation between the expression of Tim-3 on CD14(+); monocytes and serum ALT level in IA CHB patients (r=0.362, P=0.028). The levels of proinflammatory factors in supernatants, such as TNF-α, IL-1β and IL-6 increased significantly in monocytes stimulated by LPS and galectin-9, compared with ones by LPS alone.
  
  
  CONCLUSIONS
  Tim-3 expression, which is up-regulated on PBMs of CHB patients, is negatively correlated to the level of ALT in sera of IA CHB patients, and Tim-3/galectin-9 pathway might promote proinflammatory factors production of monocytes stimulated with LPS.
authors.affiliation: Department of Infectious Diseases, Affiliated Hospital, Xuzhou Medical College, Jiangsu 221002, China.
authors.forename: Xiyang
authors.initials: X
authors.lastname: Gao
authors.forename: Chan
authors.initials: C
authors.lastname: Li
authors.forename: Xiucheng
authors.initials: X
authors.lastname: Pan
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Fu
authors.forename: Wei
authors.initials: W
authors.lastname: Yao
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D037161:Galectins / Q000378:metabolism; D000072597:Hepatitis A Virus Cellular Receptor 2; D019694:Hepatitis B, Chronic / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D016130:Immunophenotyping; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017452:Receptors, IgG / Q000378:metabolism; D015398:Signal Transduction; D055815:Young Adult
chemical_list: D016207:Cytokines; D037161:Galectins; C448908:HAVCR2 protein, human; D000072597:Hepatitis A Virus Cellular Receptor 2; C105032:LGALS9 protein, human; D018950:Lipopolysaccharide Receptors; D008565:Membrane Proteins; D012333:RNA, Messenger; D017452:Receptors, IgG; D000410:Alanine Transaminase