Recognition of nucleic acids by pattern-recognition receptors and its relevance in autoimmunity

被引:170
作者
Kawasaki, Takumi [1 ]
Kawai, Taro [1 ]
Akira, Shizuo [1 ]
机构
[1] Osaka Univ, Dept Host Def, Microbial Dis Res Inst, Lab Host Def,WPI Immunol Frontier Res Ctr, Suita, Osaka 5650871, Japan
关键词
TLR; RLR; DNA sensors; autoimmune disease; PLASMACYTOID DENDRITIC CELLS; TOLL-LIKE RECEPTOR-3; INNATE IMMUNE-RESPONSE; DOUBLE-STRANDED-RNA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; AICARDI-GOUTIERES-SYNDROME; ANTIVIRAL PROTEIN VIPERIN; IFN-ALPHA PRODUCTION; ACTIVATE B-CELLS; WEST NILE VIRUS;
D O I
10.1111/j.1600-065X.2011.01048.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Host cells trigger signals for innate immune responses upon recognition of conserved structures in microbial pathogens. Nucleic acids, which are critical components for inheriting genetic information in all species including pathogens, are key structures sensed by the innate immune system. The corresponding receptors for foreign nucleic acids include members of Toll-like receptors, RIG-I-like receptors, and intracellular DNA sensors. While nucleic acid recognition by these receptors is required for host defense against the pathogen, there is a potential risk to the host of self-nucleic acids recognition, thus precipitating autoimmune and autoinflammatory diseases. In this review, we discuss the roles of nucleic acid-sensing receptors in guarding against pathogen invasion, discriminating between self and non-self, and contributing to autoimmunity and autoinflammatory diseases.
引用
收藏
页码:61 / 73
页数:13
相关论文
共 140 条
[1]   RIG-I-dependent sensing of poly(dA:dT) through the induction of an RNA polymerase III-transcribed RNA intermediate [J].
Ablasser, Andrea ;
Bauernfeind, Franz ;
Hartmann, Gunther ;
Latz, Eicke ;
Fitzgerald, Katherine A. ;
Hornung, Veit .
NATURE IMMUNOLOGY, 2009, 10 (10) :1065-U40
[2]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[3]   Type I interferon dependence of plasmacytoid dendritic cell activation and migration [J].
Asselin-Paturel, C ;
Brizard, G ;
Chemin, K ;
Boonstra, A ;
O'Garra, A ;
Vicari, A ;
Trinchieri, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 201 (07) :1157-1167
[4]   A FADD-dependent innate immune mechanism in mammalian cells [J].
Balachandran, S ;
Thomas, E ;
Barber, GN .
NATURE, 2004, 432 (7015) :401-405
[5]   Intracellular localization of Toll-like receptor 9 prevents recognition of self DNA but facilitates access to viral DNA [J].
Barton, GM ;
Kagan, JC ;
Medzhitov, R .
NATURE IMMUNOLOGY, 2006, 7 (01) :49-56
[6]   FcγRIIa is expressed on natural IFN-α-producing cells (plasmacytoid dendritic cells) and is required for the IFN-α production induced by apoptotic cells combined with lupus IgG [J].
Båve, U ;
Magnusson, M ;
Eloranta, ML ;
Perers, A ;
Alm, GV ;
Rönnblom, L .
JOURNAL OF IMMUNOLOGY, 2003, 171 (06) :3296-3302
[7]   Isolation and characterization of plasmacytoid dendritic cells from Flt3 ligand and granulocyte-macrophage colony-stimulating factor-treated mice [J].
Björck, P .
BLOOD, 2001, 98 (13) :3520-3526
[8]   The Toll-like receptor 3:dsRNA signaling complex [J].
Botos, Istvan ;
Liu, Lin ;
Wang, Yan ;
Segal, David M. ;
Davies, David R. .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, 2009, 1789 (9-10) :667-674
[9]   Toll-like receptor 9-dependent and -independent dendritic cell activation by chromatin-immunoglobulin G complexes [J].
Boulé, MW ;
Broughton, C ;
Mackay, F ;
Akira, S ;
Marshak-Rothstein, A ;
Rifkin, IR .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (12) :1631-1640
[10]   The interaction between the ER membrane protein UNC93B and TLR3, 7, and 9 is crucial for TLR signaling [J].
Brinkmann, Melanie M. ;
Spooner, Eric ;
Hoebe, Kasper ;
Beutler, Bruce ;
Ploegh, Hidde L. ;
Kim, You-Me .
JOURNAL OF CELL BIOLOGY, 2007, 177 (02) :265-275