ASAP1 gene polymorphisms are associated with susceptibility to tuberculosis in a Chinese Xinjiang Muslim population.

Seven single-nucleotide polymorphism (SNP) sites located in ASAP1 gene have been found associated with tuberculosis (TB) susceptibility by genome-wide association studies in Russia. The case-control study was carried out to test whether these seven SNPs were associated with susceptibility to TB in a Chinese Xinjiang Muslim population. The seven SNPs were genotyped in a case-control design that included 780 Xinjiang Muslim subjects (400 TB patients and 380 controls). Multiplex PCR and direct sequencing were used to detect ASAP1 gene polymorphisms. Hardy-Weinberg equilibrium test was performed to test whether the sample was from genetic equilibrium population. The associations of SNPs with TB risk were determined by the distributions of allelic frequencies and different genetic models. Significant differences of the allelic distribution of rs4733781 and rs1017281 in ASAP1 gene were observed between control group and TB group. A allele of rs4733781 was associated with TB risk (TB vs. control, OR=1.242; 95% CI: 1.004-1.537, P=0.046); While in rs1017281 site, G allele was associated with increased risk for TB (TB vs. control, OR: 0.792, 95% CI: 0.643-0.976, P=0.028). The recessive model of rs4733781 (CC vs. AC+AA) in Xinjiang Muslim populations was associated with a lower TB risk [P=0.003, OR=0.51 (0.324-0.802)], while the recessive model of rs1017281 (GG vs. AG+AA) was associated with a higher TB risk [P=0.011, OR=1.792 (1.135-2.828)]. Using case-control analysis, we identified that two genetic polymorphism sites in the ASAP1 relate to host susceptibility of TB in a Chinese Xinjiang Muslim population.

T Cell Profile was Altered in Pulmonary Tuberculosis Patients with Type 2 Diabetes.

BACKGROUND Studies have suggested that type 2 diabetes (T2D) increases the risk of active pulmonary tuberculosis (TB) infection. T2D might exacerbate TB severity and adversely impact the treatment of TB patients by suppressing the immune response of TB. However, how the immune cell profiles are changed in Chinese TB patients with coincident of T2D compared with TB patients without T2D is still unclear. MATERIAL AND METHODS To explore the immune cell profile alteration in TB patients with T2D, we collected blood samples from 46 TB patients with or without T2D and measured the profiles of T cell subsets. RESULTS We found TB patients with coincident of T2D had higher percentages of Th2 and Th17 cells after TB antigens stimulation, while they had unchanged Th1 cells and decreased CD8+ cytotoxic T cells compared to TB patients without T2D. However, no significant difference in baseline percentages of these T cells subsets was observed. CONCLUSIONS T2D has important impacts on regulating anti-TB immunity by increasing Th2 and Th17 cell differentiation, but reducing the activity of CD8+ T cells. Our study supports the need to perform longitudinal studies to evaluate the roles of immunological interaction between T2D and TB in TB development.