Innate immune recognition

被引:5963
作者
Janeway, CA
Medzhitov, R
机构
[1] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA
关键词
Toll; Drosophila; pathogen; pattern recognition; receptors;
D O I
10.1146/annurev.immunol.20.083001.084359
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 innate immune system is a universal and ancient form of host defense against infection. Innate immune recognition relies on a limited number of germline-encoded receptors. These receptors evolved to recognize conserved products of microbial metabolism produced by microbial pathogens, but not by the host. Recognition of these molecular structures allows the immune system to distinguish infectious nonself from noninfectious self. Toll-like receptors play a major role in pathogen recognition and initiation of inflammatory and immune responses. Stimulation of Toll-like receptors by microbial products leads to the activation of signaling pathways that result in the induction of antimicrobial genes and inflammatory cytokines. In addition, stimulation of Toll-like receptors triggers dendritic cell maturation and results in the induction of costimulatory molecules and increased antigen-presenting capacity. Thus, microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens.
引用
收藏
页码:197 / 216
页数:20
相关论文
共 109 条
[31]   THE TOLL GENE OF DROSOPHILA, REQUIRED FOR DORSAL-VENTRAL EMBRYONIC POLARITY, APPEARS TO ENCODE A TRANSMEMBRANE PROTEIN [J].
HASHIMOTO, C ;
HUDSON, KL ;
ANDERSON, KV .
CELL, 1988, 52 (02) :269-279
[32]   The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5 [J].
Hayashi, F ;
Smith, KD ;
Ozinsky, A ;
Hawn, TR ;
Yi, EC ;
Goodlett, DR ;
Eng, JK ;
Akira, S ;
Underhill, DM ;
Aderem, A .
NATURE, 2001, 410 (6832) :1099-1103
[33]   Resistance to endotoxin shock and reduced dissemination of gram-negative bacteria in CD14-deficient mice [J].
Haziot, A ;
Ferrero, E ;
Kontgen, F ;
Hijiya, N ;
Yamamoto, S ;
Silver, J ;
Stewart, CL ;
Goyert, SM .
IMMUNITY, 1996, 4 (04) :407-414
[34]   Relish, a central factor in the control of humoral but not cellular immunity in Drosophila [J].
Hedengren, M ;
Åsling, B ;
Dushay, MS ;
Ando, I ;
Ekengren, S ;
Wihlborg, M ;
Hultmark, D .
MOLECULAR CELL, 1999, 4 (05) :827-837
[35]   A Toll-like receptor recognizes bacterial DNA [J].
Hemmi, H ;
Takeuchi, O ;
Kawai, T ;
Kaisho, T ;
Sato, S ;
Sanjo, H ;
Matsumoto, M ;
Hoshino, K ;
Wagner, H ;
Takeda, K ;
Akira, S .
NATURE, 2000, 408 (6813) :740-745
[36]   DNA transposition by the RAG1 and RAG2 proteins: A possible source of oncogenic translocations [J].
Hiom, K ;
Melek, M ;
Gellert, M .
CELL, 1998, 94 (04) :463-470
[37]   Signaling by Toll-like receptor 2 and 4 agonists results in differential gene expression in murine macrophages [J].
Hirschfeld, M ;
Weis, JJ ;
Toshchakov, V ;
Salkowski, CA ;
Cody, MJ ;
Ward, DC ;
Qureshi, N ;
Michalek, SM ;
Vogel, SN .
INFECTION AND IMMUNITY, 2001, 69 (03) :1477-1482
[38]   Phylogenetic perspectives in innate immunity [J].
Hoffmann, JA ;
Kafatos, FC ;
Janeway, CA ;
Ezekowitz, RAB .
SCIENCE, 1999, 284 (5418) :1313-1318
[39]  
Holmskov UL, 2000, APMIS, V108, P7
[40]   TIRAP: an adapter molecule in the Toll signaling pathway [J].
Horng, T ;
Barton, GM ;
Medzhitov, R .
NATURE IMMUNOLOGY, 2001, 2 (09) :835-841