HLA DRB1, DMA, and DMB gene polymorphisms in rheumatoid arthritis

被引:11
|
作者
Reviron, D
du Montcel, ST
Foutrier, C
Guis, S
Benazet, JF
Auquier, P
Busson, M
Roux, H
Mercier, P
Roudier, J
机构
[1] Etab Tranfus Sanguine Alpes Provence, Dept Immunogenet, F-13005 Marseille, France
[2] INSERM, U155, Paris, France
[3] Fac Med Marseille, Publ Hlth Lab, F-13385 Marseille, France
[4] Hop St Louis, INSERM, U396, Paris, France
[5] La Concept Hosp, Rheumatol Ward, Marseille, France
[6] Fac Med Marseille, Immunorheumatol Dept, F-13385 Marseille, France
关键词
HLA-DRB1; HLA-DM; rheumatoid arthritis; susceptibility; linkage disequilibrium;
D O I
10.1016/S0198-8859(98)00116-5
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
OBJECTIVE: To study the influence of DMA and DMB genes on susceptibility to Rheumatoid Arthritis (RA). METHODS: HLA-DRB1, DMA and DMB polymorphisms were defined by PCR SSOP in 203 European Mediterranean RA patients and 181 unrelated healthy controls. RESULTS: No significant difference in the phenotype frequencies of DMA and DMB alleles was observed between patients and controls. We found decreased frequencies of DMA*0102 and DMB*0104 in patients but this did not reach significance. These decreased frequencies could be due to a positive linkage disequilibrium with DRB1*0701, an allele which is underrepresented in RA patients. In stratified analysis with RA susceptibility Epitope positive (SE) DRB1 alleles, there was no significant difference in DMA and DMB phenotype frequencies between SE/SE, SE/X, and X/X patients versus controls. Among SE/X subjects, no significant difference in DM distribution frequencies was observed in DRB1*0101/X, 0102/X, 0401/X, 0404/X and 0405/X groups. CONCLUSION: DMA and DMB poly morphism does not seem to influence susceptibility to develop RA. Differences in DMA phenotype frequencies between patients and controls are secondary to linkage disequilibrium with DRB1 alleles. Human Immunology 60, 245-249 (1999). (C) American Society for Histocompatibility and Immunogenetics, 1999. Published by Elsevier Science Inc.
引用
收藏
页码:245 / 249
页数:5
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