Association between the CD209 promoter −336A/G polymorphism and susceptibility to tuberculosis: A meta-analysis
Article first published online: 25 JUN 2012
© 2012 The Authors. Respirology © 2012 Asian Pacific Society of Respirology
Volume 17, Issue 5, pages 847–853, July 2012
How to Cite
MIAO, R., LI, J., SUN, Z., LI, C. and XU, F. (2012), Association between the CD209 promoter −336A/G polymorphism and susceptibility to tuberculosis: A meta-analysis. Respirology, 17: 847–853. doi: 10.1111/j.1440-1843.2012.02185.x
- Issue published online: 25 JUN 2012
- Article first published online: 25 JUN 2012
- Accepted manuscript online: 3 MAY 2012 10:33PM EST
- Received 24 October 2011; invited to revise 9 January 2012; revised 26 January 2012; accepted 16 February 2012 (Associate Editor: Robert Young)
Background and objective: Dendritic cell-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN), encoded by the CD209 gene, is a major Mycobacterium tuberculosis receptor on human dendritic cells. The potentially functional −336A/G polymorphism in the CD209 promoter region has been associated with susceptibility to tuberculosis (TB), but the results have been inconclusive. We performed a meta-analysis to clarify the relationship between the CD209−336A/G variant and the risk of TB.
Methods: Ten studies involving a total of 2598 TB patients and 2614 control subjects were systematically reviewed, and the data were quantitatively synthesized by meta-analysis. The Q-test was applied to assess the heterogeneity of associations among the studies, and Egger's regression test was used to assess potential publication bias.
Results: No significant association was identified between the CD209−336A/G polymorphism and risk of TB (G allele vs A allele: odds ratio (OR) 1.02, 95% confidence interval (CI) 0.90–1.15). Moreover, no significant association was observed in populations of African ethnicity (OR 1.01, 95% CI 0.87–1.17) or among individuals who were negative for the human immunodeficiency virus (OR 0.98, 95% CI 0.84–1.15).
Conclusions: This meta-analysis has indicated that the CD209−336A/G polymorphism may not contribute to susceptibility to TB.