Smoking, citrullination and genetic variability in the immunopathogenesis of rheumatoid arthritis

被引：192

作者：

Klareskog, Lars ^{[1
]}

Malmstrom, Vivianne ^{[1
]}

Lundberg, Karin ^{[1
]}

Padyukov, Leonid ^{[1
]}

Alfredsson, Lars ^{[2
]}

机构：

[1] Karolinska Univ Hosp, Rheumatol Unit, Dept Med, Karolinska Inst, S-17176 Stockholm, Sweden

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

来源：

SEMINARS IN IMMUNOLOGY | 2011年 / 23卷 / 02期

基金：

瑞典研究理事会;

关键词：

Rheumatoid arthritis; Autoimmunity; Citrullination; Smoking; HLA; Gene-environment interaction; Anti-CCP; GENOME-WIDE ASSOCIATION; SHARED EPITOPE ALLELES; COLLAGEN TYPE-II; ALPHA-ENOLASE; SYNOVIAL TISSUE; TRANSGENIC MICE; ANTIBODIES; PROTEIN; AUTOANTIBODIES; DISEASE;

D O I：

10.1016/j.smim.2011.01.014

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

This review describes how studies on interactions between genetic variants, and environmental factors, mainly smoking, contribute to the understanding of how autoimmunity to post-translationally (citrullinated) proteins/peptides may occur and potentially contribute to certain subsets of rheumatoid arthritis. A main message is that studies on specific immune mechanisms in a complex and heterogeneous disease like RA should be undertaken with the help of results from genetic epidemiology. By those means, it may be possible to identify subsets of RA in a way that in the end allows development and testing of precise and subset-specific interventions against environment as well as genetically defined molecular pathways, in particular those that regulate specific immune responses. (C) 2011 Published by Elsevier Ltd.

引用

页码：92 / 98

页数：7

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