ArticleBMC infectious diseases2017
G allele at -924 A > G position of FoxP3 gene promoter as a risk factor for tuberculosis.
Article in BMC infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Sex as a Biological Variable in Tuberculosis Pathogenesis.Immunological reviews · 2026Review
- Effect of immunogenetics polymorphism and expression on direct-acting antiviral drug response in chronic hepatitis C.Clinical and experimental medicine · 2024Article
- Genetic and hormonal mechanisms underlying sex-specific immune responses in tuberculosis.Trends in immunology · 2022Review
- Frequency distribution of cytokine and associated transcription factor single nucleotide polymorphisms in Zimbabweans: Impact on schistosome infection and cytokine levels.PLoS neglected tropical diseases · 2022Article
- Effect of circRNA_FOXO3 rs12196996 polymorphism and FOXO3 rs2232365 polymorphism on survival rate and severity of intensive care unit-acquired sepsis.Bioengineered · 2022Article
- Synergistic effect of genetic polymorphisms inInnate immunity · 2021Article
- FOXP3 immunoregulatory gene variants are independent predictors of human papillomavirus infection and cervical cancer precursor lesions.Journal of cancer research and clinical oncology · 2019Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundForkhead box protein 3 (FoxP3) is an important factor for development and function of Regulatory T cells (Treg). Studies have found an association between common gene polymorphisms in FoxP3 and some infectious diseases. The aim of this study was to evaluate possible associations between two Single nucleotide polymorphisms (SNPs) in the promoter of the FoxP3 gene to susceptibility to tuberculosis (TB) and the alteration of Foxp3 gene expression.
methodsThe pattern distribution of genotype at two position, -3279 A > C (rs3761548) and -924 A > G (rs2232365) on the promoter of FoxP3 gene was evaluated using polymerase chain reaction-single specific primer (PCR-SSP) method in 183 tuberculosis patients and 183 healthy control. In addition the quantity of FoxP3 gene expression at mRNA level was identified by the real-time PCR.
resultsThe frequency of G allele at -924 A > G was significantly higher was higher in TB patients (59.5%) than control group (39.5%) (P ≤ 0.05). In addition, our data viewed approximately 5- folds more FoxP3 gene expression in female patients with GG genotype in comparison to female healthy cases with the same genotype (P ≤ 0.001). There was no statistically significant differences between the distribution pattern of -3279 A > C polymorphism in patients and healthy individuals along with it effect on the FoxP3 gene expression among both groups (P > 0.05).
conclusionsOur outcome suggests that the -924 A > G polymorphism leads to enhance FoxP3 gene expression and susceptibility to tuberculosis in the sex dependent manner. This event may rise the count of Treg cells and modulate the immune response against tuberculosis.
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