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Updated: May 27, 2026
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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
CCL2−2518 (A/G) polymorphisms and tuberculosis susceptibility: a meta-analysis.
W-X Feng1, P O Flores-Villanueva, I Mokrousov
1Beijing Pediatric Research Institute, Beijing Children's Hospital affiliated to Capital Medical University, Beijing, China.
Summary
The CCL2-2518G allele is linked to a higher risk of tuberculosis (TB) in Asian and Hispanic populations. This genetic variant, specifically the CCL2 promoter polymorphism, influences susceptibility to active TB.
Area of Science:
- Genetics
- Immunology
- Epidemiology
Background:
- The -2518 C-C motif ligand (CCL)-2 promoter variant is associated with an increased risk of active tuberculosis (TB).
- Understanding genetic predispositions is crucial for TB control strategies.
Purpose of the Study:
- To investigate the association between the -2518 CCL2 gene polymorphism and susceptibility to active TB.
- To analyze the influence of this genetic variant on TB development across different ethnic groups.
Main Methods:
- A meta-analysis was performed on human genetic studies identified through Medline, PubMed, and Wan Fang databases.
- Studies published between January 1998 and November 2010 were included, focusing on the -2518 CCL2 polymorphism and active TB.
- A random effects model was utilized for the meta-analysis to synthesize findings.
Main Results:
- The CCL2-2518G allele demonstrated a significant association with increased TB susceptibility (OR 1.51).
- The recessive model (CCL2 genotype GG) showed a stronger association (OR 1.66) compared to the dominant model.
- This association was particularly evident in Asian and Hispanic populations, but not in African populations.
Conclusions:
- The CCL2-2518G allele is a risk factor for developing TB in individuals of Asian and Hispanic ancestry.
- Genetic variations in the CCL2 promoter may play a role in TB susceptibility, with population-specific effects.
- Further research is needed to explore factors like epistatic genes, environmental influences, and pathogen virulence contributing to these observed differences.
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