Does Toll-like receptor 3 play a biological role in virus infections?

被引:288
作者
Edelmann, KH
Richardson-Burns, S
Alexopoulou, L
Tyler, KL
Flavell, RA
Oldstone, MBA
机构
[1] Scripps Res Inst, Dept Neuropharmacol, Div Virol, La Jolla, CA 92037 USA
[2] Univ Colorado, Hlth Sci Ctr, Program Neurosci, Denver, CO 80262 USA
[3] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA
[4] Yale Univ, Sch Med, Howard Hughes Med Inst, Dept Internal Med, New Haven, CT 06520 USA
[5] Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO 80262 USA
[6] Univ Colorado, Hlth Sci Ctr, Dept Microbiol & Immunol, Denver, CO 80262 USA
[7] Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA
基金
美国国家卫生研究院;
关键词
Toll-like receptor 3; virus; mice;
D O I
10.1016/j.virol.2004.01.033
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The Toll-like receptor (TLR) family functions to recognize conserved microbial and viral structures with the purpose of activating signal pathways to instigate immune responses against infections by these organisms. For example, in vitro studies reveal that the TLR3 ligand is a double-stranded RNA (dsRNA), a product of viral infections. From this observation, it has been proposed that TLR3 is likely an important first signal for virus infections. We approached this issue by investigating the role of TLR3 in four different infectious viral models (lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), murine cytomegalovirus (MCMV), and reovirus) and in TLR3 genetically deficient ((-/-)) mice. Our results indicate that TLR3 is not universally required for the generation of effective antiviral responses because the absence of TLR3 does not alter either viral pathogenesis or impair host's generation of adaptive antiviral responses to these viruses. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:231 / 238
页数:8
相关论文
共 37 条
  • [1] Toll-like receptors in the induction of the innate immune response
    Aderem, A
    Ulevitch, RJ
    [J]. NATURE, 2000, 406 (6797) : 782 - 787
  • [2] SELECTION OF GENETIC-VARIANTS OF LYMPHOCYTIC CHORIOMENINGITIS VIRUS IN SPLEENS OF PERSISTENTLY INFECTED MICE - ROLE IN SUPPRESSION OF CYTO-TOXIC LYMPHOCYTE-T RESPONSE AND VIRAL PERSISTENCE
    AHMED, R
    SALMI, A
    BUTLER, LD
    CHILLER, JM
    OLDSTONE, MBA
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1984, 160 (02) : 521 - 540
  • [3] Recognition of pathogen-associated molecular patterns by TLR family
    Akira, S
    Hemmi, H
    [J]. IMMUNOLOGY LETTERS, 2003, 85 (02) : 85 - 95
  • [4] Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
    Alexopoulou, L
    Holt, AC
    Medzhitov, R
    Flavell, RA
    [J]. NATURE, 2001, 413 (6857) : 732 - 738
  • [5] BIOLOGY OF CLONED CYTO-TOXIC LYMPHOCYTES-T SPECIFIC FOR LYMPHOCYTIC CHORIOMENINGITIS VIRUS - CLEARANCE OF VIRUS AND INVITRO PROPERTIES
    ANDERSON, J
    BYRNE, JA
    SCHREIBER, R
    PATTERSON, S
    OLDSTONE, MBA
    [J]. JOURNAL OF VIROLOGY, 1985, 53 (02) : 552 - 560
  • [6] Toll signaling pathways in the innate immune response
    Anderson, KV
    [J]. CURRENT OPINION IN IMMUNOLOGY, 2000, 12 (01) : 13 - 19
  • [7] c-Jun NH2-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8+ T cell-mediated antiviral immunity
    Arbour, N
    Naniche, D
    Homann, D
    Davis, RJ
    Flavell, RA
    Oldstone, MBA
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 195 (07) : 801 - 810
  • [8] PATHOGENESIS OF MURINE CYTOMEGALOVIRUS-INFECTION IN NATURAL-KILLER CELL-DEPLETED MICE
    BUKOWSKI, JF
    WODA, BA
    WELSH, RM
    [J]. JOURNAL OF VIROLOGY, 1984, 52 (01) : 119 - 128
  • [9] IRF3 mediates a TLR3/TLR4-specific antiviral gene program
    Doyle, SE
    Vaidya, SA
    O'Connell, R
    Dadgostar, H
    Dempsey, PW
    Wu, TT
    Rao, G
    Sun, R
    Haberland, ME
    Modlin, RL
    Cheng, G
    [J]. IMMUNITY, 2002, 17 (03) : 251 - 263
  • [10] GENOMIC AND BIOLOGICAL VARIATION AMONG COMMONLY USED LYMPHOCYTIC CHORIOMENINGITIS VIRUS-STRAINS
    DUTKO, FJ
    OLDSTONE, MBA
    [J]. JOURNAL OF GENERAL VIROLOGY, 1983, 64 (AUG) : 1689 - 1698