Genes, environment and immunity in the development of rheumatoid arthritis

被引：126

作者：

Klareskog, Lars ^{[1
]}

Padyukov, Leonid

Ronnelid, Johan

Alfredsson, Lars

机构：

[1] Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden

[2] Uppsala Univ, Clin Immunol Unit, Dept Oncol Radiol & Clin Immunol, S-75105 Uppsala, Sweden

[3] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden

[4] Stockholm Cty Council, Stockholm Publ Hlth, S-10726 Stockholm, Sweden

来源：

CURRENT OPINION IN IMMUNOLOGY | 2006年 / 18卷 / 06期

关键词：

D O I：

10.1016/j.coi.2006.06.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The combined role of genes, environment and immunity in the development of rheumatoid arthritis (RA) has been the subject of recent investigations. New data support a gene-environment interaction between smoking and the MHC class II HLA-DRB1 shared epitope (SE) genes in anti-citrulline antibody (anti-CP+) RA but not in anti-CP- disease. These data from genetic epidemiology, together with information on citrullination in the lungs of smokers, have prompted the formulation of a new etiological hypothesis for anti-CP+ RA, suggesting that smoking in the context of HLA-DR SE might trigger immunity to citrulline-modified proteins and that this immunity, after several years, might cause arthritis.

引用

页码：650 / 655

页数：6

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