Innate immunity via Toll-like receptors and Nod proteins

被引:93
作者
Athman, R [1 ]
Philpott, D [1 ]
机构
[1] Inst Pasteur, F-75724 Paris 15, France
关键词
D O I
10.1016/j.mib.2003.12.013
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Host defense against microbes requires the development of an efficient immune response aimed to eradicate the source of infection. Through the expression of a battery of germ-line encoded receptors, including the Toll-like receptors and Nod proteins, the innate immune system, which is a prerequisite to the adaptive immune response, detects microbial motifs and initiates pro-inflammatory signaling. Current research into innate immune function focuses on the nature of the ligands detected by this system, the cell signaling that occurs downstream of receptor activation and finally, how these signals culminate into a tailored adaptive immune response directed to eradicate a specific infection.
引用
收藏
页码:25 / 32
页数:8
相关论文
共 56 条
  • [1] Decreased expression of toll-like receptor-4 and MD-2 correlates with intestinal epithelial cell protection against dysregulated proinflammatory gene expression in response to bacterial lipopolysaccharide
    Abreu, MT
    Vora, P
    Faure, E
    Thomas, LS
    Arnold, ET
    Arditi, M
    [J]. JOURNAL OF IMMUNOLOGY, 2001, 167 (03) : 1609 - 1616
  • [2] Bäckhed F, 2003, J INFECT DIS, V187, P829
  • [3] Toll-like receptor 4-dependent activation of dendritic cells by β-defensin 2
    Biragyn, A
    Ruffini, PA
    Leifer, CA
    Klyushnenkova, E
    Shakhov, A
    Chertov, O
    Shirakawa, AK
    Farber, JM
    Segal, DM
    Oppenheim, JJ
    Kwak, LW
    [J]. SCIENCE, 2002, 298 (5595) : 1025 - 1029
  • [4] Commensal-associated molecular patterns induce selective toll-like receptor-trafficking from apical membrane to cytoplasmic compartments in polarized intestinal epithelium
    Cario, E
    Brown, D
    McKee, M
    Lynch-Devaney, K
    Gerken, G
    Podolsky, DK
    [J]. AMERICAN JOURNAL OF PATHOLOGY, 2002, 160 (01) : 165 - 173
  • [5] Gene-environment interaction modulated by allelic heterogeneity in inflammatory diseases
    Chamaillard, M
    Philpott, D
    Girardin, SE
    Zouali, H
    Lesage, S
    Chareyre, F
    Bui, TH
    Giovannini, M
    Zaehringer, U
    Penard-Lacronique, V
    Sansonetti, PJ
    Hugot, JP
    Thomas, G
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (06) : 3455 - 3460
  • [6] Chamaillard M, 2003, NAT IMMUNOL, V4, P702, DOI 10.1038/ni945
  • [7] Nods, Nalps and Naip: intracellular regulators of bacterial-induced inflammation
    Chamaillard, M
    Girardin, SE
    Viala, J
    Philpott, DJ
    [J]. CELLULAR MICROBIOLOGY, 2003, 5 (09) : 581 - 592
  • [8] Requirement for a peptidoglycan recognition protein (PGRP) in relish activation and antibacterial immune responses in Drosophila
    Choe, KM
    Werner, T
    Stöven, S
    Hultmark, D
    Anderson, KV
    [J]. SCIENCE, 2002, 296 (5566) : 359 - 362
  • [9] Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction
    Fitzgerald, KA
    Palsson-McDermott, EM
    Bowie, AG
    Jefferies, CA
    Mansell, AS
    Brady, G
    Brint, E
    Dunne, A
    Gray, P
    Harte, MT
    McMurray, D
    Smith, DE
    Sims, JE
    Bird, TA
    O'Neill, LAJ
    [J]. NATURE, 2001, 413 (6851) : 78 - 83
  • [10] LPS-TLR4 signaling to IRF-3/7 and NF-κB involves the toll adapters TRAM and TRIF
    Fitzgerald, KA
    Rowe, DC
    Barnes, BJ
    Caffrey, DR
    Visintin, A
    Latz, E
    Monks, B
    Pitha, PM
    Golenbock, DT
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (07) : 1043 - 1055