The role of interferon-gamma in the increased tuberculosis risk in type 2 diabetes mellitus

Eur J Clin Microbiol Infect Dis. 2008 Feb;27(2):97-103. doi: 10.1007/s10096-007-0395-0. Epub 2007 Oct 26.


As patients with diabetes mellitus are at increased risk of developing tuberculosis, we hypothesized that this susceptibility to mycobacterial infection is due to a defective Th1-cytokine response. To explore this hypothesis, we examined four groups of subjects in Indonesia: 23 patients with tuberculosis, 34 patients with tuberculosis and diabetes, 32 patients with diabetes only and 36 healthy controls. Ex-vivo production of interferon (IFN)gamma, tumour necrosis factor-alpha and interleukin (IL)-1beta, 6, 10, -12 and -4 was measured following stimulation with Mycobacterium tuberculosis, Escherichia coli lipopolysaccharide and phytohaemagglutinin. Patients with active tuberculosis were found to have lower IFNgamma levels and a higher production of other pro-inflammatory cytokines and IL-4, both in the presence and absence of diabetes. Diabetes patients without tuberculosis, however, showed strongly reduced non-specific IFNgamma production, which is essential for inhibition of the initial growth of M. tuberculosis. Our data suggest that a defective non-specific immune response in diabetes may contribute to an increased susceptibility to develop tuberculosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cells, Cultured
  • Diabetes Complications / immunology*
  • Diabetes Mellitus, Type 2 / immunology*
  • Disease Susceptibility / immunology
  • Female
  • Humans
  • Indonesia
  • Interferon-gamma / immunology*
  • Leukocytes, Mononuclear / immunology
  • Male
  • Middle Aged
  • Risk
  • Tuberculosis / immunology*


  • Interferon-gamma