Association between the CD209 promoter −336A/G polymorphism and susceptibility to tuberculosis: A meta-analysis

ABSTRACT 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 regi...

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Veröffentlicht in:Respirology (Carlton, Vic.) Vic.), 2012-07, Vol.17 (5), p.847-853
Hauptverfasser: MIAO, RUIFEN, LI, JIEQUAN, SUN, ZHAOPING, LI, CHEN, XU, FEI
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Sprache:eng
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Zusammenfassung:ABSTRACT 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. Meta‐analysis of 10 association studies has indicated that the CD209−336A/G promoter polymorphism may not contribute to susceptibility to tuberculosis.
ISSN:1323-7799
1440-1843
DOI:10.1111/j.1440-1843.2012.02185.x