Inferences, questions and possibilities in toll-like receptor signalling

被引:1200
作者
Beutler, B [1 ]
机构
[1] Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/nature02761
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The Toll-like receptors (TLRs) are the key proteins that allow mammals-whether immunologically naive or experienced-to detect microbes. They lie at the core of our inherited resistance to disease, initiating most of the phenomena that occur in the course of infection. Quasi-infectious stimuli that have been used for decades to study inflammatory mechanisms can activate the TLR family of proteins. And it now seems that many inflammatory processes, both sterile and infectious, may depend on TLR signalling. We are in a good position to apply our understanding of TLR signalling to a range of challenges in immunology and medicine.
引用
收藏
页码:257 / 263
页数:7
相关论文
共 87 条
[61]   Toll-like receptor (TLR) 2 and TLR4 are essential for Aspergillus-induced activation of murine macrophages [J].
Meier, A ;
Kirschning, CJ ;
Nikolaus, T ;
Wagner, H ;
Heesemann, J ;
Ebel, F .
CELLULAR MICROBIOLOGY, 2003, 5 (08) :561-570
[62]   Therapeutic targeting of Toll-like receptors for inflammatory and infectious diseases [J].
O'Neill, LA .
CURRENT OPINION IN PHARMACOLOGY, 2003, 3 (04) :396-403
[63]   Physical contact between lipopolysaccharide and Toll-like receptor 4 revealed by genetic complementation [J].
Poltorak, A ;
Ricciardi-Castagnoli, P ;
Citterio, S ;
Beutler, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (05) :2163-2167
[64]   Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice:: Mutations in Tlr4 gene [J].
Poltorak, A ;
He, XL ;
Smirnova, I ;
Liu, MY ;
Van Huffel, C ;
Du, X ;
Birdwell, D ;
Alejos, E ;
Silva, M ;
Galanos, C ;
Freudenberg, M ;
Ricciardi-Castagnoli, P ;
Layton, B ;
Beutler, B .
SCIENCE, 1998, 282 (5396) :2085-2088
[65]   INSECT IMMUNITY - DEVELOPMENTAL AND INDUCIBLE ACTIVITY OF THE DROSOPHILA DIPTERICIN PROMOTER [J].
REICHHART, JM ;
MEISTER, M ;
DIMARCQ, JL ;
ZACHARY, D ;
HOFFMANN, D ;
RUIZ, C ;
RICHARDS, G ;
HOFFMANN, JA .
EMBO JOURNAL, 1992, 11 (04) :1469-1477
[66]   TRAF2-MEDIATED ACTIVATION OF NF-KAPPA-B BY TNF RECEPTOR-2 AND CD40 [J].
ROTHE, M ;
SARMA, V ;
DIXIT, VW ;
GOEDDEL, DV .
SCIENCE, 1995, 269 (5229) :1424-1427
[67]   The Rel protein DIF mediates the antifungal but not the antibacterial host defense in Drosophila [J].
Rutschmann, S ;
Jung, AC ;
Hetru, C ;
Reichhart, JM ;
Hoffmann, JA ;
Ferrandon, D .
IMMUNITY, 2000, 12 (05) :569-580
[68]   IκB kinases phosphorylate NF-κB p65 subunit on serine 536 in the transactivation domain [J].
Sakurai, H ;
Chiba, H ;
Miyoshi, H ;
Sugita, T ;
Toriumi, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (43) :30353-30356
[69]   Functional interactions of transforming growth factor β-activated kinase 1 with IκB kinases to stimulate NF-κB activation [J].
Sakurai, H ;
Miyoshi, H ;
Toriumi, W ;
Sugita, T .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (15) :10641-10648
[70]   Toll-like receptors control activation of adaptive immune responses [J].
Schnare, M ;
Barton, GM ;
Holt, AC ;
Takeda, K ;
Akira, S ;
Medzhitov, R .
NATURE IMMUNOLOGY, 2001, 2 (10) :947-950