期刊文献+

Analysis of MIF,FCGR2A and FCGR3A gene polymorphisms with susceptibility to pulmonary tuberculosis in Moroccan population 被引量:4

Analysis of MIF,FCGR2A and FCGR3A gene polymorphisms with susceptibility to pulmonary tuberculosis in Moroccan population
原文传递
导出
摘要 In order to investigate the influence of functional polymorphisms of macrophage migration inhibitory factor (M/F), Fcg receptors CD16A (FCGR3A) and CD32A (FCGR2A) genes on susceptibility to pulmonary tuberculosis (PTB) in the Moroccan population, we analyzed 123 patients with PTB and 154 healthy controls. The genotyping for M/F-173 (G/C) (rs755622), FCGR2A- 131H/R (rs 1801274) and FCGR3A-158V/F (rs396991) was carried out using TaqMan SNP Genotyping Assay method. We found a statistically significant in- crease of the MIF-173CC homozygote genotype and M/F-173"C allele frequencies in PTB patients compared with healthy controls (17.07% versus 5.84%, P = 0.003; and 35.37% versus 26.30%, P = 0.02; respectively). In contrast, no association was observed between FCGR2A-131H/R and FCGR3A-158V/F polymorphisms and tuberculosis disease. Our finding suggests that M/F-173℃ variant may play an important role in the development of active tuberculosis. In order to investigate the influence of functional polymorphisms of macrophage migration inhibitory factor (M/F), Fcg receptors CD16A (FCGR3A) and CD32A (FCGR2A) genes on susceptibility to pulmonary tuberculosis (PTB) in the Moroccan population, we analyzed 123 patients with PTB and 154 healthy controls. The genotyping for M/F-173 (G/C) (rs755622), FCGR2A- 131H/R (rs 1801274) and FCGR3A-158V/F (rs396991) was carried out using TaqMan SNP Genotyping Assay method. We found a statistically significant in- crease of the MIF-173CC homozygote genotype and M/F-173"C allele frequencies in PTB patients compared with healthy controls (17.07% versus 5.84%, P = 0.003; and 35.37% versus 26.30%, P = 0.02; respectively). In contrast, no association was observed between FCGR2A-131H/R and FCGR3A-158V/F polymorphisms and tuberculosis disease. Our finding suggests that M/F-173℃ variant may play an important role in the development of active tuberculosis.
出处 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2010年第4期257-264,共8页 遗传学报(英文版)
基金 supported in part by the grants SAF06-00398/CTS1880,Spain in another part by the National Institute of Hygiene,Rabat,Morocco
关键词 FCGR MIF POLYMORPHISM SUSCEPTIBILITY pulmonary tuberculosis MOROCCAN FCGR MIF polymorphism susceptibility pulmonary tuberculosis Moroccan
  • 相关文献

参考文献48

  • 1Bacher, M., Metz, C.N., Calandra, T., Mayer, K., Chesney, J., Lohoff, M., Gemsa, D., Donnelly, T., and Bucala, R. (1996). An essential regulatory role for macrophage migration inhibitory factor in T-cell activation. Proc. Natl. Acad. Sci. USA 93: 7849-7854.
  • 2Barton, A., Lamb, R., Symmons, D., Silman, A., Thomson, W., Worthingtonl, J., and Donn, R. (2003). Macrophage migration inhibitory factor (M/F) gene polymorphism is associated with susceptibility to but not severity of inflammatory polyarthritis. Genes Immun. 4: 487-491.
  • 3Baugh, J.A., Chitnis, S., Donnelly, S.C., Monteiro, J., Lin, X., Plant, B.J., Wolfe, F., Gregersen, P.K., and Bucala, R. (2002). A functional promoter polymorphism in the macrophage migration inhibitory factor (M/F) gene associated with disease severity in rheumatoid arthritis. Genes Immun. 3: 170-176.
  • 4Bellamy, R. (2003). Susceptibility to mycobacterial infections: the importance of host genetics. Genes Immun. 4:4-11.
  • 5Biezeveld, M., Geissler, J., Merkus, M., Kuipers, I.M., Ottenkamp, J., and Kuijpers, T. (2006). The involvement of Fc gamma receptor gent polymorphisms in Kawasaki disease. Clin. Exp. Immunol. 147: 106-111.
  • 6Bloom, B.R., and Bennett, B. (1966). Mechanism of a reaction in vitro associated with delayed-type hypersensitivity. Science 153: 80-82.
  • 7Calandra, T. (2003). Macrophage migration inhibitory factor and host innate immune responses to microbes. Scand. J. Infect. Dis. 35: 573-576.
  • 8Casanova, ,I.L., and Abel, L. (2002). Genetic dissection of immunity to mycobacteria: the human model. Annu. Rev. Immunol. 20:581-620.
  • 9Dambacher, J., Staudinger, T., Seiderer, J., Sisic, Z., Schnitzler, F., Pfennig, S., Hofbauer, K., Konrad, A., Tillack, C., Otte, J.M., Diebold, J., G6ke, B., Ochsenkiihn, T., Lohse, P., and Brand, S. (2007). Macrophage migration inhibitory factor (MIF) -173G/C Promoter polymorphism influences upper gastrointestinal tract involvement and disease activity in patients with crohn's disease, Inflamm. Bowel Dis. 13: 71-82.
  • 10David, J.R. (1966). Delayed hypersensitivity in vitro: its mediation by cell-free substances formed by lymphoid cell-antigen interaction. Proc. Natl. Acad. Sci. USA 56: 72-77.

同被引文献17

引证文献4

二级引证文献24

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部