title: Circulating IL-2 and IL-10 in chronic active hepatitis C with respect to the response to IFN treatment.
abstract: BACKGROUND
  The importance of circulating immunoregulatory cytokines in response to IFN treatment and the change of in vivo production of these cytokines during interferon (IFN) treatment are not well known. We aimed to determine whether pretreatment serum levels of IL-2 and IL-10 are predictive of the response to IFN treatment and to investigate if treatment response or nonresponse has any effect on the circulating levels of these cytokines.
  
  
  METHODS
  37 patients (18 responders and 19 non-responders) with chronic hepatitis C virus (HCV) infection who received IFN-alpha2b for 6 months were studied. Responders were defined by complete alanine aminotransferase (ALT) normalization and loss of HCV RNA as detected by bDNA assay while patients who had elevated ALT levels and positive HCV RNA after 6 months were considered as nonresponders.
  
  
  RESULTS
  Genotype distribution, ALT and HCV RNA levels were similar in responders and nonresponders. A significant number of patients with chronic hepatitis C (20/37 = 54%) had elevated IL-2 levels while IL-10 levels were not different from controls. No difference in baseline cytokine levels was observed between responders and non-responders. In the posttreatment serum samples some patients lost their detectable IL-2 or IL-10; some patients developed detectable cytokine levels after treatment irrespective of the treatment response.
  
  
  CONCLUSIONS
  These results suggest that active liver injury in chronic hepatitis C is associated with increased circulating Th1 cytokine IL-2 but not with Th2 cytokine IL-10 and that circulating levels of these cytokines do not predict the response to IFN treatment. There is no constant and regular change in circulating levels of these cytokines under IFN treatment with respect to treatment response.
authors.affiliation: Ankara University, Dept. of Gastroenteroloygy, Cebeci Tip Fakültesi, Dikimevi, Turkey. bozkaya@dirlup.ankara.edu.tr
authors.forename: H
authors.initials: H
authors.lastname: Bozkaya
authors.forename: A M
authors.initials: AM
authors.lastname: Bozdayi
authors.forename: N
authors.initials: N
authors.lastname: Aslan
authors.forename: C
authors.initials: C
authors.lastname: Türkay
authors.forename: M
authors.initials: M
authors.lastname: Sarioglu
authors.forename: H
authors.initials: H
authors.lastname: Cetinkaya
authors.forename: M
authors.initials: M
authors.lastname: Akdogan
authors.forename: K
authors.initials: K
authors.lastname: Cinar
authors.forename: E
authors.initials: E
authors.lastname: Erden
authors.forename: K
authors.initials: K
authors.lastname: Köse
authors.forename: H
authors.initials: H
authors.lastname: Sentürk
authors.forename: H
authors.initials: H
authors.lastname: Akkiz
authors.forename: S
authors.initials: S
authors.lastname: Karayalcin
authors.forename: C
authors.initials: C
authors.lastname: Yurdaydin
authors.forename: O
authors.initials: O
authors.lastname: Uzunalimoglu
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000097:blood / Q000628:therapy* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000097:blood*; D007376:Interleukin-2 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins; D013997:Time Factors
chemical_list: D000077190:Interferon alpha-2; D016898:Interferon-alpha; D007376:Interleukin-2; D012367:RNA, Viral; D011994:Recombinant Proteins; D016753:Interleukin-10; D000410:Alanine Transaminase