Genetic epidemiology of rheumatoid arthritis

被引：31

作者：

Oliver, JE ^{[1
]}

Worthington, J ^{[1
]}

Silman, AJ ^{[1
]}

机构：

[1] Univ Manchester, Sch Epidemiol & Hlth Sci, Epidemiol Unit, Manchester M13 9PT, Lancs, England

来源：

CURRENT OPINION IN RHEUMATOLOGY | 2006年 / 18卷 / 02期

关键词：

CTLA-4; cytokine; FCRL3; human leukocyte antigen; MHC2TA; outcome; PADI4; PTPN22; treatment;

D O I：

10.1097/01.bor.0000209425.84775.23

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Purpose of review This review aims to summarize articles published between October 2004 and November 2005 that have investigated the genetic epidemiology of rheumatoid arthritis. Recent findings The consistent replication of an association between the R620W single nucleotide polymorphism in PTPN22 and rheumatoid arthritis clearly establishes this polymorphism as an important risk factor for rheumatoid arthritis. Summary Genetic investigations of rheumatoid arthritis have predominantly been single nucleotide polymorphism-based candidate gene association studies searching for markers of susceptibility, severity or treatment response. Studies of the human leukocyte antigen region have refined and added to our understanding of the complex associations to polymorphisms with this locus. PTPN22 has emerged strongly as a genuine rheumatoid arthritis susceptibility gene with replications of the association to the R620W single nucleotide polymorphism. Many investigations have been conducted on the genetics of treatment response some 'generic' and others specific in terms of identifying genetic influences to the mode of action and metabolism of particular agents.

引用

页码：141 / 146

页数：6

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