The role of Toll-like receptors in chronic inflammation

被引:199
|
作者
Drexler, Stefan K. [1 ]
Foxwell, Brian M. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst, Div Rheumatol, London W6 8LH, England
关键词
Autoimmune diseases; Toll-like receptor; Inflammation; NF-KAPPA-B; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; PROSTATE-CANCER RISK; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELOID DIFFERENTIATION FACTOR-88; ARTHRITIS SYNOVIAL FIBROBLASTS; NASOPHARYNGEAL CARCINOMA RISK; AIRWAY EPITHELIAL-CELLS; RHEUMATOID-ARTHRITIS;
D O I
10.1016/j.biocel.2009.10.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The role of Toll-like receptors (TLRs) in innate immunity and their ability to recognise microbial products has been well characterised. TLRs are also able to recognise endogenous molecules which are released upon cell damage and necrosis and have been shown to be present in numerous autoimmune diseases. Therefore, the release of endogenous TLR ligands during inflammation and consequently the activation of TLR signalling pathways may be one mechanism initiating and driving autoimmune diseases. An increasing body of circumstantial evidence implicates a role of TLR signalling in systemic lupus erythematosus (SLE), atherosclerosis, asthma, type 1 diabetes, multiple sclerosis, bowl inflammation and rheumatoid arthritis (RA). Although at present their involvement is not comprehensively defined. However, future therapies targeting individual TLRs or their signalling transducers may provide a more specific way of treating inflammatory diseases without global suppression of the immune system. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:506 / 518
页数:13
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