Genetic susceptibility to SLE: new insights from fine mapping and genome-wide association studies

被引:220
作者
Harley, Isaac T. W. [1 ,2 ,3 ]
Kaufman, Kenneth M. [1 ,4 ,5 ]
Langefeld, Carl D. [6 ]
Harley, John B. [1 ,4 ,5 ]
Kelly, Jennifer A. [1 ]
机构
[1] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA
[2] Cincinnati Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH USA
[3] Univ Cincinnati, Coll Med PSTP, Cincinnati, OH USA
[4] Oklahoma City US Dept, Vet Affairs Med Ctr, Oklahoma City, OK 73104 USA
[5] Univ Oklahoma, Coll Med, Oklahoma City, OK 73104 USA
[6] Wake Forest Univ Hlth Sci, Sect Stat Genet & Bioinformat, Winston Salem, NC USA
基金
美国国家卫生研究院;
关键词
SYSTEMIC-LUPUS-ERYTHEMATOSUS; TYROSINE-PHOSPHATASE; FUNCTIONAL VARIANTS; REVISED CRITERIA; RISK-FACTOR; PTPN22; POLYMORPHISMS; INTERFERON; CLASSIFICATION; EXPRESSION;
D O I
10.1038/nrg2571
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Genome-wide association studies and fine mapping of candidate regions have rapidly advanced our understanding of the genetic basis of systemic lupus erythematosus (SLE). More than 20 robust associations have now been identified and confirmed, providing insights at the molecular level that refine our understanding of the involvement of host immune response processes. In addition, genes with unknown roles in SLE pathophysiology have been identified. These findings may provide new routes towards improved clinical management of this complex disease.
引用
收藏
页码:285 / 290
页数:6
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