Toll-like receptors as adjuvant receptors

被引:376
作者
Kaisho, T [1 ]
Akira, S [1 ]
机构
[1] Osaka Univ, Microbial Dis Res Inst, Dept Host Defense, Suita, Osaka 5650871, Japan
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2002年 / 1589卷 / 01期
关键词
Toll-like receptor; adjuvant; dendritic cell; lipopolysaccharide; MyD88; innate immunity;
D O I
10.1016/S0167-4889(01)00182-3
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 mammalian Toll-like receptors (TLRs) are expressed on macrophages and dendritic cells, which are primarily involved in innate immunity. At present, ligands for several of the TLRs, such as TLR2, TLR3, TLR4, TLR5, TLR6, and TLR9, have been identified. Most of these ligands are derived from pathogens, but not found in the host, suggesting that the TLRs are critical to sensing invading microorganisms. Pathogen recognition by TLRs provokes rapid activation of innate immunity by inducing production of proinflammatory cytokines and upregulation of costimulatory molecules. Activated innate immunity subsequently leads to effective adaptive immunity. In this regard, the TLRs are considered to be adjuvant receptors. Distinct TLRs can exert distinct, but overlapping sets of biological effects. Accumulating evidence indicates that this can be attributed to both the common and unique aspects of the signaling mechanisms that mediate TLR family responses. For example, TLR2 and TLR9 require MyD88 as an essential signal transducer, whereas TLR4 can induce costimulatory molecule upregulation in a MyD88-independent manner. Understanding the TLR system should offer invaluable opportunity for manipulating host immune responses. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:1 / 13
页数:13
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