Joint first authors.
Genome-wide haplotype association analysis and gene prioritization identify CCL3 as a risk locus for rheumatoid arthritis
Article first published online: 27 MAY 2010
© 2010 Blackwell Publishing Ltd
International Journal of Immunogenetics
Volume 37, Issue 4, pages 273–278, August 2010
How to Cite
Zhang, R., Sun, P., Jiang, Y., Chen, Z., Huang, C., Zhang, X. and Zhang, R. (2010), Genome-wide haplotype association analysis and gene prioritization identify CCL3 as a risk locus for rheumatoid arthritis. International Journal of Immunogenetics, 37: 273–278. doi: 10.1111/j.1744-313X.2010.00920.x
- Issue published online: 29 JUN 2010
- Article first published online: 27 MAY 2010
- Received 31 August 2009; revised 25 December 2009; accepted 25 March 2010
Rheumatoid arthritis (RA) is a common autoimmune disease caused by a complex interaction of multiple genetic variants and environmental factors. The association between RA and genetic susceptibility loci has been observed in many different populations, and most studies have focused on univariate analyses of single nucleotide polymorphisms. We performed a genome-wide haplotype association study and prioritized RA-related genes within 100 kb in either direction of significant haplotypes (P < 0.0001), based on their similarity to known RA susceptibility genes. The results showed that the chemokine CCL3 was associated with susceptibility to RA. A haplotype that located CCL3 on chromosome 17q12 had significant correlation with RA (P = 7.56E-05), and the global similarity score of CCL3 was ranked in the top of all RA-related genes, excluding known susceptibility genes (P = 8.42E-07). Our findings provide further evidence for the potential importance of the chemokine CCL3 in RA, and will facilitate the further understanding of its role in immunological regulation and the pathogenesis of RA.