The role of Toll-like receptors in host defense against microbial infection

被引:110
作者
Krutzik, SR [1 ]
Sieling, PA [1 ]
Modlin, RL [1 ]
机构
[1] Univ Calif Los Angeles, Sch Med, Inst Mol Biol, Dept Microbiol & Immunol,Dept Med,Div Dermatol, Los Angeles, CA 90095 USA
关键词
D O I
10.1016/S0952-7915(00)00189-8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The Toll family of proteins is central to Drosophila host defense against microbial infection. Maintained throughout evolution, mammalian Toll-like receptors (TLRs) are proteins that participate in innate immunity to bacteria in at least four ways. First, TLRs participate in the recognition of molecular patterns present on microorganisms. Second, TLRs are expressed at the interface with the environment, the site of microbial invasion. Third, activation of TLRs induces expression of co-stimulatory molecules and the release of cytokines that instruct the adaptive immune response. Fourth, activation of TLRs leads to direct antimicrobial effector pathways that can result in elimination of the foreign invader. The recent investigation of TLRs in these areas has provided new insights into mechanisms of innate immunity.
引用
收藏
页码:104 / 108
页数:5
相关论文
共 53 条
[31]   Cutting edge: Endotoxin tolerance in mouse peritoneal macrophages correlates with down-regulation of surface Toll-like receptor 4 expression [J].
Nomura, F ;
Akashi, S ;
Sakao, Y ;
Sato, S ;
Kawai, T ;
Matsumoto, M ;
Nakanishi, K ;
Kimoto, M ;
Miyake, K ;
Takeda, K ;
Akira, S .
JOURNAL OF IMMUNOLOGY, 2000, 164 (07) :3476-3479
[32]  
OBRIEN AD, 1980, J IMMUNOL, V124, P20
[33]   The toll-like receptor protein RP105 regulates lipopolysaccharide signaling in B cells [J].
Ogata, H ;
Su, I ;
Miyake, K ;
Nagai, Y ;
Akashi, S ;
Mecklenbräuker, I ;
Rajewsky, K ;
Kimoto, M ;
Tarakhovsky, A .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (01) :23-29
[34]   Heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex [J].
Ohashi, K ;
Burkart, V ;
Flohé, S ;
Kolb, H .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :558-561
[35]   The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between Toll-like receptors [J].
Ozinsky, A ;
Underhill, DM ;
Fontenot, JD ;
Hajjar, AM ;
Smith, KD ;
Wilson, CB ;
Schroeder, L ;
Aderem, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (25) :13766-13771
[36]   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
[37]   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
[38]   PU.1 and interferon consensus sequence-binding protein regulate the myeloid expression of the human toll-like receptor 4 gene [J].
Rehli, M ;
Poltorak, A ;
Schwarzfischer, L ;
Krause, SW ;
Andreesen, R ;
Beutler, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (13) :9773-9781
[39]   Anti-human RP105 sera induces lymphocyte proliferation [J].
Roshak, AK ;
Anderson, KM ;
Holmes, SD ;
Jonak, Z ;
Bolognese, B ;
Terrett, J ;
Marshall, LA .
JOURNAL OF LEUKOCYTE BIOLOGY, 1999, 65 (01) :43-49
[40]   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