Viral recognition by the innate immune system: the role of pattern recognition receptors

被引:0
作者
Torres Pedraza, Silvia [1 ,2 ]
Guillermo Betancur, Juan [2 ,3 ]
Urcuqui-Inchima, Silvio [2 ]
机构
[1] Univ Antioquia, Corp Ciencias Basicas Biomed, Medellin, Colombia
[2] Univ Antioquia, Sede Invest Univ, Immunovirol Grp, Medellin, Colombia
[3] Univ Tokyo, Inst Mol & Cellular Biosci, Tokyo 1138654, Japan
来源
COLOMBIA MEDICA | 2010年 / 41卷 / 04期
关键词
Innate immunity; Pro-inflammatory cytokines; Toll-like receptors; RIG-I-like receptors; NF-KAPPA-B; RIG-I; HUMAN MONOCYTES; RNA HELICASE; VIRUS; ACTIVATION; PROTEIN; CELLS; INTERFERENCE; INVOLVEMENT;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pattern recognition receptors are the main sensors of the innate immune response. Their function is to recognize pathogen-associated molecular patterns, which are molecules essential for the survival of microbial pathogens, but are not produced by the host. The recognition of pathogen-associated molecular patterns by pattern recognition receptors leads to the expression of cytokines, chemokines, and co-stimulatory molecules that eliminate pathogens, such as viruses, for the activation of antigen presenting cells and for the activation of specific adaptive immunity. Among the most thoroughly studied pattern recognition receptors implicated in viral infections, there are the toll-like receptors (TLRs) and the RNA helicase-type retinoic acid-inducible gene-1 receptors [or RIG-like receptors (RLRs)]. Moreover, other proteins such as PKR, 2'-5' OAS, and ADAR also act as effector proteins in antiviral responses. The identification and characterization of pattern recognition receptors have contributed to our knowledge of the role of innate immunity in viral infections and has led us to better understand host-pathogen interactions. The most recent findings concerning the role of TLRs and RLRs in viral infections, the molecular mechanisms of viral ligand recognition through pattern recognition receptors, and the activation of their signaling pathways are discussed in this review. Colomb Med. 2010; 41: 377-87
引用
收藏
页码:377 / 387
页数:11
相关论文
共 60 条
[1]   Recognition of pathogen-associated molecular patterns by TLR family [J].
Akira, S ;
Hemmi, H .
IMMUNOLOGY LETTERS, 2003, 85 (02) :85-95
[2]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[3]   The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-β promoter [J].
Andrejeva, J ;
Childs, KS ;
Young, DF ;
Carlos, TS ;
Stock, N ;
Goodbourn, S ;
Randall, RE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (49) :17264-17269
[4]   Production of type I interferons: plasmacytoid dendritic cells and beyond [J].
Asselin-Paturel, C ;
Trinchieri, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (04) :461-465
[5]   Hemagglutinin protein of wild-type measles virus activates Toll-like receptor 2 signaling [J].
Bieback, K ;
Lien, E ;
Klagge, IM ;
Avota, E ;
Schneider-Schaulies, J ;
Duprex, WP ;
Wagner, H ;
Kirschning, CJ ;
ter Meulen, V ;
Schneider-Schaulies, S .
JOURNAL OF VIROLOGY, 2002, 76 (17) :8729-8736
[6]   A46R and A52R from vaccinia virus are antagonists of host IL-1 and toll-like receptor signaling [J].
Bowie, A ;
Kiss-Toth, E ;
Symons, JA ;
Smith, GL ;
Dower, SK ;
O'Neill, LAJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (18) :10162-10167
[7]   Identification of the rabies virus alpha/beta interferon antagonist:: Phosphoprotein P interferes with phosphorylation of interferon regulatory factor 3 [J].
Brzózka, K ;
Finke, S ;
Conzelmann, KK .
JOURNAL OF VIROLOGY, 2005, 79 (12) :7673-7681
[8]   Human cytomegalovirus activates inflammatory cytokine responses via CD14 and toll-like receptor 2 [J].
Compton, T ;
Kurt-Jones, EA ;
Boehme, KW ;
Belko, J ;
Latz, E ;
Golenbock, DT ;
Finberg, RW .
JOURNAL OF VIROLOGY, 2003, 77 (08) :4588-4596
[9]   Transcriptional activation of alpha/beta interferon genes: Interference by nonsegmented negative-strand RNA viruses [J].
Conzelmann, KK .
JOURNAL OF VIROLOGY, 2005, 79 (09) :5241-5248
[10]   IL-12 receptor β1 and Toll-like receptor 4 increase IL-1β- and IL-18-associated myocarditis and Coxsackievirus replication [J].
Fairweather, D ;
Yusung, S ;
Frisancho, S ;
Barrett, M ;
Gatewood, S ;
Steele, R ;
Rose, NR .
JOURNAL OF IMMUNOLOGY, 2003, 170 (09) :4731-4737