Meta-analysis of the Association between HLA-DRB1 Allele and Rheumatoid Arthritis Susceptibility in Asian Populations.
10.3346/jkms.2007.22.6.973
- Author:
Kyung Ran JUN
1
;
Sung Eun CHOI
;
Choong Hwan CHA
;
Heung Bum OH
;
Yong Seok HEO
;
Hong Yup AHN
;
Kwan Jeh LEE
Author Information
1. Department of Laboratory Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. hboh@amc.seoul.kr
- Publication Type:Original Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
- Keywords:
Arthritis, Rheumatoid;
Genetics;
Epitopes;
HLA-DRB1;
Meta-analysis;
Asian Continental Ancestry Group
- MeSH:
*Alleles;
Arthritis, Rheumatoid/*genetics;
Asian Continental Ancestry Group/*genetics;
*Genetic Predisposition to Disease;
HLA-DR Antigens/chemistry/*genetics;
Humans
- From:Journal of Korean Medical Science
2007;22(6):973-980
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aims of this study were to summarize results on the association of HLA-DRB1 with rheumatoid arthritis (RA) in Asians and to determine if the shared epitope (SE) hypothesis could explain the meta-analysis results. Among the papers published between January 1987 and July 2006 on RA susceptibility in Asian-Mongoloid populations (Korean, Japanese, Chinese, and Thai), 12 were selected for the metaanalysis. Mongoloid-Asian patients with RA had significantly higher frequencies of HLA-DRB1*0101, *0401, *0410, and *1001 than controls (OR 1.5-2.1, p<0.05 for association). When analyses were restricted to more ethnically homogeneous populations, HLA-DRB1*0405 showed a significant susceptibility to RA in Koreans (OR 5.65, 95% CI 4.32-7.39), whereas the HLA-DRB1*0301, *0403, *0406, *0701, *1301, and *1405 alleles showed protective association with RA (OR 0.32-0.70, p<0.05 for association). In conclusion, it was found that HLA-DRB1 *0101, *0401, *0405, *0410, and *1001 are susceptible, while HLA-DRB1* 0301, *0403, *0406, *0701, *1301, and *1405 are protective in Asian-Mongoloids. All the RA-associated alleles except DRB1*0301 could be explained by the structural model supporting the SE hypothesis that RA susceptibility is determined by the combination of amino acid residues at HLA-DR beta71 and beta74, not by beta71 alone.
