title: [ALLELE POLYMORPHISM OF THE IFNG AND TGFB GENES AS A FACTOR OF MODULATION OF CYTOKINE SECRETION AND SUSCEPTIBILITY TO PULMONARY TUBERCULOSIS].
abstract: By applying the current immunological and molecular genetic studies, the authors revealed a genetically determined imbalance in the pro- duction of immunoregulatory cytokines by monoluclear leukocytes in pulmonary tuberculosis. T allele and TT genotype of IFNG gene poly- morphism +874A/T were found to be an immunogenetic factor that had a protective effect against susceptibility to pulmonary tuberculosis. Susceptibility to tuberculosis infection is associated with A allele and with AA and AT genotypes of IFNG gene polymorphism +874A/T and the CTpolymorphic variant G509Tof the TGFB gene. The maximum risk for pulmonary tuberculosis is associated with a combination of the AA genotypes of the polymorphic site +874A/Tof the IFNG gene and TT polymorphism G509T of the TGFB gene (AA/TT).
mesh_terms: D000328:Adult; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease; D006239:Haplotypes; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D016212:Transforming Growth Factor beta / Q000235:genetics*; D014397:Tuberculosis, Pulmonary / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines; C573415:IFNG protein, human; D016212:Transforming Growth Factor beta; D007371:Interferon-gamma