Associations between cytotoxic T lymphocyte-associated antigen-4 polymorphisms and serum tumor necrosis factor-α and interferon-γ levels in patients with chronic hepatitis B virus infection

Inflamm Res. 2011 Nov;60(11):1071-8. doi: 10.1007/s00011-011-0368-8. Epub 2011 Aug 17.

Abstract

Background: Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) polymorphism, which may affect host immune response including cytokines production, is thought to be associated with hepatitis B virus (HBV) infection. This study investigated the associations between CTLA4 polymorphism and serum tumor necrosis factor (TNF)-α and interferon (IFN)-γ levels in patients with chronic HBV infection.

Methods: CTLA4 promoter -318C/T and exon 1 +49A/G polymorphisms and serum TNF-α and IFN-γ levels were determined in 172 patients with chronic HBV infection and 145 healthy controls.

Results: The genotype of CTLA4 -318C/T polymorphism had no association to TNF-α and IFN-γ levels. Serum levels of TNF-α and IFN-γ in chronic HBV patients with +49GG genotype were lower than those with +49AG genotype (p = 0.030 and p = 0.042, respectively), and haplotypes -318C + 49A and -318C + 49G seemed to have no significant effects on TNF-α and IFN-γ levels.

Conclusions: CTLA4 +49GG genotype was associated to lower TNF-α and IFN-γ levels in patients with chronic HBV infection but this association was diminished by haplotype formation with -318C/T alleles, indicating that the influence of CTLA4 -318C/T and +49A/G polymorphisms on the susceptibility and disease progress of chronic HBV infection may not be effectuated by affecting TNF-α and IFN-γ secretion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Alleles
  • CTLA-4 Antigen / blood
  • CTLA-4 Antigen / genetics*
  • Exons
  • Female
  • Genotype
  • Haplotypes
  • Hepatitis B virus / metabolism*
  • Hepatitis B, Chronic / blood*
  • Hepatitis B, Chronic / virology*
  • Humans
  • Interferon-gamma / blood*
  • Male
  • Middle Aged
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic
  • Tumor Necrosis Factor-alpha / blood*

Substances

  • CTLA-4 Antigen
  • CTLA4 protein, human
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma