类风湿关节炎中不存在对HLA - DQ编码易感性的支持。
No support for HLA-DQ encoded susceptibility in rheumatoid arthritis.
作者信息
de Vries N, van Elderen C, Tijssen H, van Riel P L, van de Putte L B
机构信息
Department of Rheumatology, University Hospital Nijmegen, The Netherlands.
出版信息
Arthritis Rheum. 1999 Aug;42(8):1621-7. doi: 10.1002/1529-0131(199908)42:8<1621::AID-ANR9>3.0.CO;2-0.
OBJECTIVE
To test predictions based on data from immunogenetic and peptide-binding studies of collagen-induced arthritis in mice, in which it has been suggested that susceptibility to rheumatoid arthritis (RA) might be determined by the interaction between susceptibility alleles at the HLA-DQ locus and protective alleles at the HLA-DRB1 locus (including susceptibility effects for HLA-DQ7 and DQ8).
METHODS
Predictions based on these models were tested in 166 healthy controls and 167 patients with RA, all of whom were typed for HLA-DRB1 and HLA-DQ alleles.
RESULTS
In this population, HLA-DQ7 did not encode an increased risk for RA. This lack of susceptibility effect of HLA-DQ7 could not be attributed to competing HLA-DQ susceptibility alleles, protective HLA-DRB1 alleles, or the absence of DQA1*0301.
CONCLUSION
These observations do not support the DR/DQ hypothesis in its present form.
目的
基于小鼠胶原诱导性关节炎的免疫遗传学和肽结合研究数据进行预测检验，研究表明类风湿关节炎（RA）易感性可能由HLA - DQ位点的易感等位基因与HLA - DRB1位点的保护等位基因之间的相互作用决定（包括HLA - DQ7和DQ8的易感效应）。
方法
在166名健康对照者和167名RA患者中对基于这些模型的预测进行检验，所有受试者均进行了HLA - DRB1和HLA - DQ等位基因分型。
结果
在该人群中，HLA - DQ7并未编码增加的RA风险。HLA - DQ7缺乏易感效应不能归因于竞争性HLA - DQ易感等位基因、保护性HLA - DRB1等位基因或DQA1*0301的缺失。
结论
这些观察结果不支持目前形式的DR/DQ假说。
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