title: The expression kinetics of CD137 in chronic hepatitis C patients treated with pegylated-interferon and ribavirin.
abstract: OBJECTIVE
  CD137, a member of the tumor necrosis factor receptor family, generates co-stimulatory signals leading to T-cell activation and proliferation for viral eradication. We examined the expression kinetics of CD137 to validate whether it can affect treatment outcomes of chronic hepatitis C (CHC) patients.
  
  
  METHODS
  The expression of CD137 on peripheral blood mononuclear cells (PBMC) from 50 CHC patients and 20 healthy controls was analyzed by flow cytometry. CD137 expression levels were examined before treatment, and every 4 weeks during treatment until week 24 or 48, and at the 24-week follow-up.
  
  
  RESULTS
  CD137 expression on PBMC was significantly lower in CHC patients than controls (15.5 ± 7.8% vs 23.4 ± 5.2%; p < 0.05). Patients with sustained virological response (SVR) showed higher level of CD137 expression on PBMC than treatment failures at week 4 (20.11% vs 10.97%; p < 0.05) and week 12 (15.48% vs 5.74%; p < 0.01). CD137 expression on CD4 T cells was also higher in patients with SVR at week 8 (7.75% vs 3.29%; p < 0.05). CD137 expression on PBMC from patients with SVR recovered to the control level at the 24-week follow-up. In multivariate analysis, the increased expression of CD137 at week 4 and genotype non-1 were significantly associated with SVR.
  
  
  CONCLUSIONS
  The increased expression of CD137 within 12 weeks after the initiation of interferon therapy might be associated with a successful treatment outcome. Modulation to improve expression of CD137 might improve efficacy of CHC treatment.
authors.affiliation: Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Korea.
authors.forename: Sang Jin
authors.initials: SJ
authors.lastname: Lee
authors.forename: Jung Woo
authors.initials: JW
authors.lastname: Shin
authors.forename: Bo Ryung
authors.initials: BR
authors.lastname: Park
authors.forename: Chang Jae
authors.initials: CJ
authors.lastname: Kim
authors.forename: Seok Won
authors.initials: SW
authors.lastname: Jung
authors.forename: Byunggyu
authors.initials: B
authors.lastname: Kim
authors.forename: In Du
authors.initials: ID
authors.lastname: Jeong
authors.forename: Sung-Jo
authors.initials: SJ
authors.lastname: Bang
authors.forename: Neung Hwa
authors.initials: NH
authors.lastname: Park
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D016001:Confidence Intervals; D005260:Female; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000378:metabolism* / Q000821:virology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use; D018709:Statistics, Nonparametric; D013997:Time Factors; D016896:Treatment Outcome; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9 / Q000378:metabolism*; D019562:Viral Load; D055815:Young Adult
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D011994:Recombinant Proteins; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a