Association study of polymorphisms in interferon-γ receptor genes with the risk of pulmonary tuberculosis

Mol Med Rep. 2015 Jul;12(1):1568-78. doi: 10.3892/mmr.2015.3544. Epub 2015 Mar 24.

Abstract

Tuberculosis (TB) is an infectious disease caused by mycobacterium, which most commonly affects the lungs. The adaptive immune response in Mycobacterium tuberculosis is predominantly mediated by the interferon-γ (IFN-γ) signaling pathway, which is regulated by IFN-γ receptors (IFNGR). IFN-γ activates the transcription of a number of genes that are important in immune responses, thus the appropriate function of IFNGR appears to be important in host defense against mycobacteria. In the present study, 22 genetic variants in IFNGR1 and IFNGR2 were genotyped in 673 patients and 592 normal controls to investigate the association between IFNGR1 and IFNGR2 polymorphisms and the risk of TB. Statistical analyses revealed that four genetic variants in IFNGR1, rs9376269, rs9376268, rs9376267 and rs56251346 were marginally associated with the risk of TB (P = 0.02-0.04), while other single nucleotide polymorphisms in IFNGR1 and IFNGR2 did not exhibit any associations. However, the significance of the four genetic variants rs9376269, rs9376268, rs9376267 and rs56251346 was eliminated following a multiple testing correction of the data (P>0.05). The present results revealed that certain genetic variants in IFNGR genes may be associated with TB development, which may be useful preliminary data for future investigation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Female
  • Genetic Association Studies*
  • Genetic Predisposition to Disease
  • Humans
  • Interferon gamma Receptor
  • Male
  • Middle Aged
  • Mycobacterium tuberculosis / genetics
  • Mycobacterium tuberculosis / immunology
  • Mycobacterium tuberculosis / pathogenicity
  • Polymorphism, Single Nucleotide
  • Receptors, Interferon / genetics*
  • Receptors, Interferon / immunology
  • Tuberculosis, Pulmonary / genetics*
  • Tuberculosis, Pulmonary / immunology
  • Tuberculosis, Pulmonary / microbiology

Substances

  • IFNGR2 protein, human
  • Receptors, Interferon