The contribution of toll-like receptors to the pathogenesis of asthma

被引:46
|
作者
Phipps, Simon
Lam, Chuan En
Foster, Paul S.
Matthaei, Klaus I.
机构
[1] Australian Natl Univ, John Curtin Sch Med Res, Gene Targeting Lab, Canberra, ACT 0200, Australia
[2] Univ Newcastle, Sch Biomed Sci, CARD, Newcastle, NSW 2308, Australia
[3] Hunter Med Res, Vaccines Immun Viruses & Asthma Grp, Newcastle, NSW, Australia
来源
IMMUNOLOGY AND CELL BIOLOGY | 2007年 / 85卷 / 06期
关键词
asthma; pathogenesis; toll-like receptors;
D O I
10.1038/sj.icb.7100104
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Asthma is a major disease in the westernized world and its incidence has significantly increased over the past 40 years. Our understanding of the pathogenesis of asthma remains rudimentary, and for this reason, little has been accomplished by way of targeted intervention, either at a population level ( to reduce the overall prevalence) or at an individual level ( to treat the cause). Instead, the management strategy currently in use relies on broad-spectrum anti-inflammatory agents, generally glucocorticoids and long-acting beta 2 agonists. The recent discovery of toll-like receptors (TLRs), with their role as the initiators of the innate immune response and inflammation, suggests that modulating these receptors may be beneficial in the treatment of allergic disorders. We review here the cellular distribution of TLR in the lung and their potential contribution to the processes that promote T helper 2 (Th2) immunity and infection-induced exacerbations of allergic lung disease.
引用
收藏
页码:463 / 470
页数:8
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