title: Circulating IL-2, IL-10 and TNF-alpha in chronic hepatitis B: their relations to HBeAg status and the activity of liver disease.
abstract: OBJECTIVE
  Preferential production of immunoregulatory cytokines may play an important role in the pathogenesis of chronic hepatitis B. We aimed to determine the serum levels of IL-2, IL-10 and TNF-alpha in patients with chronic hepatitis B and to correlate these findings with the activity of liver disease, HBeAg/anti-HBe status and replication level of the virus.
  
  
  METHODS
  Seventy-two chronic hepatitis B patients were categorized into 4 groups according to activity of liver disease and HBeAg status. Group 1 (n = 13): HBeAg and HBV DNA-positive with persistently normal ALT. Group 2 (n = 20): HBeAg and HBV DNA-positive patients with persistently elevated ALT. Group 3 (n = 19): HBeAg and HBV DNA-negative patients with persistently normal ALT. Group 4 (n = 20): HBeAg-negative patients with persistently elevated ALT and variable serum HBV DNA. IL-2, IL-10 and TNFa levels were determined in stored patient sera.
  
  
  RESULTS
  Apart from group 1 patients, all patients groups had higher IL-2 levels compared to controls suggesting that IL-2 production is increased when liver disease becomes active in HBeAg-positive phase of HBV infection. Only group 2 patients had elevated IL-10 levels compared to controls. None of the HBeAg-negative patients had detectable TNF-alpha levels while 64% HBeAg-positive patients had elevated levels of TNF-alpha irrespective of the activity of liver disease. Except TNF-alpha, no association was found between HBV DNA status and the presence or absence of detectable cytokines in circulation.
  
  
  CONCLUSIONS
  Our results suggest that circulating cytokine profile in chronic hepatitis B is related with the HBeAg status, replication level of the virus and the activity of liver disease.
authors.affiliation: Ankara University, School of Medicine, Department of Gastroenterology, Turkey. bozkaya@dialup.ankara.edu.tr
authors.forename: H
authors.initials: H
authors.lastname: Bozkaya
authors.forename: M
authors.initials: M
authors.lastname: Bozdayi
authors.forename: R
authors.initials: R
authors.lastname: Türkyilmaz
authors.forename: M
authors.initials: M
authors.lastname: Sarioglu
authors.forename: H
authors.initials: H
authors.lastname: Cetinkaya
authors.forename: K
authors.initials: K
authors.lastname: Cinar
authors.forename: K
authors.initials: K
authors.lastname: Köse
authors.forename: C
authors.initials: C
authors.lastname: Yurdaydin
authors.forename: O
authors.initials: O
authors.lastname: Uzunalimoglu
mesh_terms: D000293:Adolescent; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D016207:Cytokines / Q000097:blood*; D004279:DNA, Viral / Q000097:blood; D005260:Female; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019562:Viral Load
chemical_list: D016207:Cytokines; D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D000410:Alanine Transaminase