title: Serum interleukin 4 and interleukin 10 levels in patients with chronic hepatitis C virus infection.
abstract: OBJECTIVE
  Immune-mediated mechanisms are believed to play an important pathogenetic role in chronic hepatitis C virus infection. Interleukin 4 (IL-4) and IL-10 are secreted by T helper-2 type cells (Th2) which may downregulate cell-mediated immune effector mechanisms important in the host defense against intracellular pathogens. This study aimed to determine Th2 cytokine levels in chronic hepatitis C virus infection.
  
  
  METHODS
  Serum IL-4 and IL-10 levels were measured in 74 patients with chronic hepatitis C virus infection and 20 healthy controls. The expression of CD30 in liver, a marker that is preferentially expressed in Th2 cells, was also determined by immunohistochemical staining in 37 patients.
  
  
  RESULTS
  Serum IL-4 and IL-10 were below the detection limit (5 pg/ml) in all 20 healthy controls. However, 36 patients (49%) had elevated serum IL-4 levels (range 5-106 pg/ml, p<0.001) and 23 patients (31%) had elevated serum IL-10 levels (range 5-37 pg/ml, p<0.05). There was no correlation between serum IL-4 and IL-10 levels. There was also no correlation between serum IL-4 and IL-10 levels and any of the clinical (age, gender, mode of acquisition), biochemical (serum alanine transaminase levels), virologic (viremia level, genotype), and histological parameters examined. Twenty of 37 liver biopsy specimens from patients with chronic hepatitis C virus infection showed occasional CD30+ lymphocytes, suggestive of Th2 phenotype. However, in 20 of the 37 patients with paired cryostat liver sections, IL-4 was not detected in any of these patients, suggesting that IL-4 was not produced in the liver in patients with chronic hepatitis C virus infection.
  
  
  CONCLUSIONS
  This study showed that serum Th2 cytokines are elevated (but at a low level) in a proportion of patients with chronic hepatitis C virus infection. However, the elevated Th2 cytokine levels may represent a systemic response and not a result of increased local production within the liver.
authors.affiliation: Department of Medicine, University of Florida, Gainesville 32610, USA.
authors.forename: M
authors.initials: M
authors.lastname: Reiser
authors.forename: C G
authors.initials: CG
authors.lastname: Marousis
authors.forename: D R
authors.initials: DR
authors.lastname: Nelson
authors.forename: G
authors.initials: G
authors.lastname: Lauer
authors.forename: R P
authors.initials: RP
authors.lastname: González-Peralta
authors.forename: G L
authors.initials: GL
authors.lastname: Davis
authors.forename: J Y
authors.initials: JY
authors.lastname: Lau
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D000956:Antigens, Viral / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002908:Chronic Disease; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016753:Interleukin-10 / Q000097:blood*; D015847:Interleukin-4 / Q000097:blood*; D017730:Ki-1 Antigen / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012313:RNA / Q000737:chemistry; D012367:RNA, Viral / Q000032:analysis; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000956:Antigens, Viral; D015415:Biomarkers; D017730:Ki-1 Antigen; C034477:RNA primers; D012367:RNA, Viral; D016753:Interleukin-10; D015847:Interleukin-4; D012313:RNA; D000410:Alanine Transaminase