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日本人群中DMA和DMB与类风湿关节炎的关联。

Association of DMA and DMB with RA in Japanese.

作者信息

Takeuchi F, Nabeta H, Kuwata S, Tanimoto K, Ito K

机构信息

Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Clin Exp Rheumatol. 1997 Mar-Apr;15(2):189-92.

PMID:9196873
Abstract

OBJECTIVE

The contribution of polymorphism of DMA and DMB alleles to the pathogenesis of Japanese RA was studied. The association of DM alleles with HLA-DRB1*0405 and *0802, which were positively and negatively susceptible to Japanese RA, respectively, is also discussed.

METHODS

DMA and DMB typing was carried out in 91 Japanese RA patients and in 77 normal subjects by the PCR-RFLP (restriction fragment length polymorphism) method. HLA-DRB1*04 and *08 genotyping were carried out by the PCR-SSCP (single-stranded DNA conformation polymorphism) method.

RESULTS

Allele frequencies of DMB0101 and DMB0102 were slightly higher (52.2% and 27.0%) and the allele frequency of DMB0103 was slightly lower (25.8%) in RA, but these differences were not significant. The increase of DMB0102 was due to a negative association with HLA-DRB10802 [p < 0.05, pc = not significant (NS)]. The decrease of DMB0103 was due to a positive association with DRB10802 (p < 0.005, pc < 0.05). The increase of DMB0101 was possibly due to a weak association with HLA-DRB1*0405, (p = NS). Positivity of rheumatoid factor did not affect the prevalence of DMA and DMB alleles.

CONCLUSION

Association analysis among DMA, DMB and DRB1 (0405 and 0802) indicate that slight increases or decreases in DMB0101, DMB0102 and DMB0103 are not primary indicators but reflect an increase in HLA-DRB1 0405 and a decrease in HLA-DRB1*0802 in Japanese RA.

摘要

目的

研究DMA和DMB等位基因多态性对日本类风湿关节炎(RA)发病机制的影响。还讨论了DM等位基因与HLA - DRB10405和0802的关联,这两个基因分别对日本RA呈正易感性和负易感性。

方法

采用PCR - RFLP(限制性片段长度多态性)方法对91例日本RA患者和77例正常受试者进行DMA和DMB分型。采用PCR - SSCP(单链DNA构象多态性)方法进行HLA - DRB104和08基因分型。

结果

在RA患者中,DMB0101和DMB0102的等位基因频率略高(分别为52.2%和27.0%),而DMB0103的等位基因频率略低(25.8%),但这些差异无统计学意义。DMB0102的增加是由于与HLA - DRB10802呈负相关[p < 0.05,校正P值=无显著性差异(NS)]。DMB0103的减少是由于与DRB10802呈正相关(p < 0.005,校正P值< 0.05)。DMB0101的增加可能是由于与HLA - DRB1*0405的弱关联(p = NS)。类风湿因子阳性不影响DMA和DMB等位基因的患病率。

结论

DMA、DMB和DRB1(0405和0802)之间的关联分析表明,DMB0101、DMB0102和DMB0103的轻微增减不是主要指标,而是反映了日本RA患者中HLA - DRB10405的增加和HLA - DRB1*0802的减少。

相似文献

1
Association of DMA and DMB with RA in Japanese.日本人群中DMA和DMB与类风湿关节炎的关联。
Clin Exp Rheumatol. 1997 Mar-Apr;15(2):189-92.
2
HLA-DMA and DMB genotyping in patients with rheumatoid arthritis.类风湿关节炎患者的HLA - DMA和DMB基因分型
J Rheumatol. 1997 Mar;24(3):442-4.
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Hum Immunol. 2000 Mar;61(3):303-8. doi: 10.1016/s0198-8859(99)00126-3.
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HLA DRB1, DMA, and DMB gene polymorphisms in rheumatoid arthritis.类风湿关节炎中的HLA DRB1、DMA和DMB基因多态性
Hum Immunol. 1999 Mar;60(3):245-9. doi: 10.1016/s0198-8859(98)00116-5.
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HLA-DMA*0103 and HLA-DMB*0104 alleles as novel prognostic factors in rheumatoid arthritis.HLA-DMA*0103和HLA-DMB*0104等位基因作为类风湿关节炎的新预后因素。
Ann Rheum Dis. 2004 Dec;63(12):1581-6. doi: 10.1136/ard.2003.012294.
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Positive association of the HLA DMB1*0101-0101 genotype with rheumatoid arthritis.HLA DMB1*0101-0101基因型与类风湿关节炎呈正相关。
Rheumatology (Oxford). 1999 May;38(5):448-52. doi: 10.1093/rheumatology/38.5.448.
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Association of DM genes in systemic sclerosis is secondary to the association with HLA genes.系统性硬化症中糖尿病相关基因的关联是继发于与HLA基因的关联。
Scand J Rheumatol. 1997;26(3):174-9. doi: 10.3109/03009749709065677.
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Polymorphisms of DMA and DMB genes in Japanese systemic lupus erythematosus.日本系统性红斑狼疮患者中DMA和DMB基因的多态性
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HLA DMA and DMB show no association with rheumatoid arthritis in US Caucasians.在美国白种人中,HLA DMA和DMB与类风湿性关节炎无关联。
Eur J Immunogenet. 2001 Oct;28(5):539-43. doi: 10.1046/j.1365-2370.2001.00258.x.
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Polymorphism of the HLA-DMA and DMB genes in rheumatoid arthritis.类风湿关节炎中HLA - DMA和DMB基因的多态性
Arthritis Rheum. 1997 May;40(5):854-8. doi: 10.1002/art.1780400512.

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Ann Rheum Dis. 2004 Dec;63(12):1645-8. doi: 10.1136/ard.2003.015552.
2
HLA-DMA*0103 and HLA-DMB*0104 alleles as novel prognostic factors in rheumatoid arthritis.HLA-DMA*0103和HLA-DMB*0104等位基因作为类风湿关节炎的新预后因素。
Ann Rheum Dis. 2004 Dec;63(12):1581-6. doi: 10.1136/ard.2003.012294.