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Abstract
Aim. The present study was undertaken to find out the possible association between interferon-gamma (IFN-γ) receptor 1 (IFNGR1) gene polymorphisms and risk of pulmonary tuberculosis (PTB) in a sample of Iranian population. Methods. Polymorphisms of IFNGR1 rs1327474 (−611 A/G), rs11914 (+189 T/G), rs7749390 (+95 C/T), and rs137854905 (27-bp ins/del) were determined in 173 PTB patients and 164 healthy subjects. Results. Our findings showed that rs11914 TG genotypes decreased the risk of PTB in comparison with TT (OR = 0.36, 95% CI = 0.21–0.62, and p = 0.0002). The rs11914 G allele decreased the risk of PTB compared with T allele (OR = 0.41, 95% CI = 0.25–0.68, and p = 0.0006). IFNGR1 rs7749390 CT genotype decreased the risk of PTB in comparison with CC genotype (OR = 0.55, 95% CI = 0.32–0.95, and p = 0.038). No significant association was found between IFNGR1 rs1327474 A/G polymorphism and risk/protective of PTB. The rs137854905 (27-bp I/D) variant was not polymorphic in our population. Conclusion. Our findings showed that IFNGR1 rs11914 and rs7749390 variants decreased the risk of PTB susceptibility in our population.
Highlights
Tuberculosis is an infectious disease and remains a major public health problem as well as leading cause of morbidity and mortality worldwide mostly in Asia and Africa [1, 2]
It has been proposed that IFNG can activate murine macrophages to inhibit M. tuberculosis growth [21]
Our previous study indicated an association between IFNG +874 T/A polymorphism and susceptibility to pulmonary tuberculosis (PTB) [5]
Summary
Tuberculosis is an infectious disease and remains a major public health problem as well as leading cause of morbidity and mortality worldwide mostly in Asia and Africa [1, 2]. It has been expected that one-third of population is infected with TB, while 5–10% of infected cases will develop active TB during their lifetimes [3], which suggests a role of genetic variation in host immunity. It was expected that the impact of genetic factors on the phenotypic variation and immune responses in the population infected with TB ranges up to 71% [4]. IFNG and its receptor (IFNGR1) are key components of innate and adaptive immunity and have been involved in a wide range of infectious and inflammatory disease processes. The α subunit (encoded by the gene IFNGR1) plays a critical role in ligand binding, receptor trafficking, and signal transduction [13]. The IFNGR1 gene is located on the long arm of chromosome 6 at position 23.3 (6q23.3), which encodes the ligand binding chain (alpha) of the interferon-gamma receptor. Defects in IFNGR1 have been reported as a cause of Mendelian susceptibility to mycobacterial disease, known as familial disseminated atypical mycobacterial infection [14]
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