GENETIC AND EPIGENETIC REGULATION OF IFN-g; IN PATIENTS WITH ACTIVE TUBERCULOSIS

ESTERMANN MARTIN; ALVAREZ GUADALUPE INES; BARBERO ANGELA MARIA; CELANO JOSEFINA; PASQUINELLI VIRGINIA

Hannover

Congreso; 6th Lower Saxony International Summer Academy in Immunology; 2016

Despite the wide variety of anti-tuberculosis drugs and significant progress made in treatment administration with improved control strategies in response to the global tuberculosis epidemic, tuberculosis (TB) remains an important health problem worldwide. Although more than one-third of the world?s population is potentially infected with M. tuberculosis, only 10 % of infected individuals eventually develop TB disease, indicating that host genetic factors may play essential but complex role in determining susceptibility and progression to TB disease. The response triggered by IFN-g is a key component for the generation of a protective immune response against M. tuberculosis. A significant association between +874A/T (rs2430561) single nucleotide polymorphism (SNP) in IFNG and protection against TB has been demonstrated in several populations. In addition, epigenetic mechanisms may also influence gene expression. It has been reported that in vitro methylation of -53 CpG site of IFN-g promoter markedly reduces binding of transcription factors and is key in the transcriptional regulation of this gene (Jones B, et al. EMBO J, 2006).