Innate immunity to mycobacterial infection in mice: Critical role for toll-like receptors

被引:50
作者
Ryffel, B [1 ]
Fremond, C
Jacobs, M
Parida, S
Botha, T
Schnyder, B
Quesniaux, V
机构
[1] CNRS, IEM2815, F-45071 Orleans, France
[2] Univ Cape Town, Inst Infect Dis & Mol Med, ZA-7925 Cape Town, South Africa
[3] Armauer Hansen Res Inst, Addis Ababa, Ethiopia
[4] Cape Technikon, Cape Town, South Africa
[5] Biomed Res Fdn, Matzingen, Switzerland
关键词
toll-like receptor; mycobacteria; innate and adaptive immunity;
D O I
10.1016/j.tube.2005.08.021
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Toll-like receptors (TLRs) play a critical role in the recognition of several pathogens, including Mycobacterium, tuberculosis. Mycobacterial antigens recognize distinct TLRs resulting in rapid activation of cells of the innate immune system. Ablation of most of the TLR signalling as in mice deficient for the common adaptor protein MyD88 reveals that TLR is crucial for the activation of an innate immune response. MyD88-deficient mice are unable to clear virulent mycobacteria and succumb to acute necrotic pneumonia. Despite the profound defect of the innate immune response, MyD88 deficiency allows the emergence of an adaptive immunity. These data demonstrate that activation of multiple TLRs contributes to an efficient innate response to mycobacteria, while MyD88-dependent signalling is dispensable to generate adaptive immunity. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:395 / 405
页数:11
相关论文
共 112 条
[1]   Toll-like receptor 4 expression is required to control chronic Mycobacterium tuberculosis infection in mice [J].
Abel, B ;
Thieblemon, N ;
Quesniaux, VJF ;
Brown, N ;
Mpagi, J ;
Miyake, K ;
Bihl, F ;
Ryffel, B .
JOURNAL OF IMMUNOLOGY, 2002, 169 (06) :3155-3162
[2]   Mammalian Toll-like receptors [J].
Akira, S .
CURRENT OPINION IN IMMUNOLOGY, 2003, 15 (01) :5-11
[3]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[4]   Role of adapters in Toll-like receptor signalling [J].
Akira, S ;
Yamamoto, M ;
Takeda, K .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2003, 31 :637-642
[5]   Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 [J].
Aliprantis, AO ;
Yang, RB ;
Mark, MR ;
Suggett, S ;
Devaux, B ;
Radolf, JD ;
Klimpel, GR ;
Godowski, P ;
Zychlinsky, A .
SCIENCE, 1999, 285 (5428) :736-739
[6]  
BARNES PF, 1992, J IMMUNOL, V149, P541
[7]   Reactivation of latent tuberculosis infection in TNF-deficient mice [J].
Botha, T ;
Ryffel, B .
JOURNAL OF IMMUNOLOGY, 2003, 171 (06) :3110-3118
[8]   Toll-like receptor 4 plays a protective role in pulmonary tuberculosis in mice [J].
Branger, J ;
Leemans, JC ;
Florquin, S ;
Weijer, S ;
Speelman, P ;
van der Poll, T .
INTERNATIONAL IMMUNOLOGY, 2004, 16 (03) :509-516
[9]   Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors [J].
Brightbill, HD ;
Libraty, DH ;
Krutzik, SR ;
Yang, RB ;
Belisle, JT ;
Bleharski, JR ;
Maitland, M ;
Norgard, MV ;
Plevy, SE ;
Smale, ST ;
Brennan, PJ ;
Bloom, BR ;
Godowski, PJ ;
Modlin, RL .
SCIENCE, 1999, 285 (5428) :732-736
[10]   Dectin-1 is a major β-glucan receptor on macrophages [J].
Brown, GD ;
Taylor, PR ;
Reid, DM ;
Willment, JA ;
Williams, DL ;
Martinez-Pomares, L ;
Wong, SYC ;
Gordon, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 196 (03) :407-412