Accelerated telomere shortening in rheumatic diseases: cause or consequence?

被引：22

作者：

Dehbi, Amina Z. A. ^{[1
]}

Radstake, Timothy R. D. J. ^{[1
,2
]}

Broen, Jasper C. A. ^{[1
,2
]}

机构：

[1] Univ Med Ctr Utrecht, Lab Translat Immunol, NL-3584 EA Utrecht, Netherlands

[2] Univ Med Ctr Utrecht, Dept Rheumatol & Clin Immunol, NL-3584 EA Utrecht, Netherlands

来源：

EXPERT REVIEW OF CLINICAL IMMUNOLOGY | 2013年 / 9卷 / 12期

关键词：

osteoarthritis; rheumatoid arthritis; SLE; systemic sclerosis; T cells; telomeres;

D O I：

10.1586/1744666X.2013.850031

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：

Accelerated aging of the immune system (immune aging), represented by telomere shortening, has been implicated in a variety of rheumatic diseases. Studies addressing telomere shortening in rheumatic diseases so far yielded controversial results. The current review aims to provide an overview on the role of immune aging in a plethora of immune-mediated conditions including systemic sclerosis, rheumatoid arthritis, systemic lupus erythematosus and osteoarthritis. The main question this review aims to answer is whether rheumatic diseases cause accelerated aging or that accelerated aging drives rheumatic diseases.

引用

页码：1193 / 1204

页数：12

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