Renal Toll-like receptors: recent advances and implications for disease

被引:48
作者
El-Achkar, Tarek M. [1 ]
Dagher, Pierre C. [1 ]
机构
[1] Indiana Univ, Dept Med, Div Nephrol, Indiana Ctr Biol Microscopy, Indianapolis, IN 46202 USA
来源
NATURE CLINICAL PRACTICE NEPHROLOGY | 2006年 / 2卷 / 10期
关键词
glomerulonephritis; inflammation; ischemia; renal failure; sepsis;
D O I
10.1038/ncpneph0300
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Toll-like receptors (TLRs) are proteins that recognize specific molecular patterns of pathogens. They can also interact with a variety of endogenous ligands. When stimulated, TLRs initiate a cascade of signaling events leading to the production of a myriad of cytokines and effector molecules. Early investigations extensively characterized TLRs on cells of the innate immune system. More recently, TLRs have been found to reside in organs such as the heart, lungs, intestines, liver and kidneys. The role of these TLRs is not fully understood and is the subject of intensive current research. The available information indicates that renal TLRs have the potential to interact with exogenous and endogenous ligands, thereby influencing kidney function in health and disease. Here, we present an overview of what is currently known about renal TLRs, and discuss the potential implications for further research and clinical practice.
引用
收藏
页码:568 / 581
页数:14
相关论文
共 149 条
[51]   Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway [J].
Hemmi, H ;
Kaisho, T ;
Takeuchi, O ;
Sato, S ;
Sanjo, H ;
Hoshino, K ;
Horiuchi, T ;
Tomizawa, H ;
Takeda, K ;
Akira, S .
NATURE IMMUNOLOGY, 2002, 3 (02) :196-200
[52]   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
[53]   The interface between innate and adaptive immunity [J].
Hoebe, K ;
Janssen, E ;
Beutler, B .
NATURE IMMUNOLOGY, 2004, 5 (10) :971-974
[54]   Upregulation of costimulatory molecules induced by lipopolysaccharide and double-stranded RNA occurs by Trif-dependent and Trif-independent pathways [J].
Hoebe, K ;
Janssen, EM ;
Kim, SO ;
Alexopoulou, L ;
Flavell, RA ;
Han, JH ;
Beutler, B .
NATURE IMMUNOLOGY, 2003, 4 (12) :1223-1229
[55]  
Hoshino K, 1999, J IMMUNOL, V162, P3749
[56]   Medical progress: The pathophysiology and treatment of sepsis. [J].
Hotchkiss, RS ;
Karl, IE .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (02) :138-150
[57]   Association study of Toll-like receptor 9 gene polymorphism in Korean patients with systemic lupus erythematosus [J].
Hur, JW ;
Shin, HD ;
Park, BL ;
Kim, LH ;
Kim, SY ;
Bae, SC .
TISSUE ANTIGENS, 2005, 65 (03) :266-270
[58]   Receptor-mediated monitoring of tissue well-being via detection of soluble heparan sulfate by toll-like receptor 4 [J].
Johnson, GB ;
Brunn, GJ ;
Kodaira, Y ;
Platt, JL .
JOURNAL OF IMMUNOLOGY, 2002, 168 (10) :5233-5239
[59]   Human TLR7 or TLR8 independently confer responsiveness to the antiviral compound R-848 [J].
Jurk, M ;
Heil, F ;
Vollmer, J ;
Schetter, C ;
Krieg, AM ;
Wagner, H ;
Lipford, G ;
Bauer, S .
NATURE IMMUNOLOGY, 2002, 3 (06) :499-499
[60]   Apoptosis induced by the toll-like receptor adaptor TRIF is dependent on its receptor interacting protein homotypic interaction motif [J].
Kaiser, WJ ;
Offermann, MK .
JOURNAL OF IMMUNOLOGY, 2005, 174 (08) :4942-4952