Inflammasomes in inflammatory disorders: The role of TLRs and their interactions with NLRs

被引:137
作者
Becker, Christine E. [1 ]
O'Neill, Luke A. J. [1 ]
机构
[1] Univ Dublin Trinity Coll, Sch Biochem & Immunol, Dublin 2, Ireland
关键词
TLR; NLR; PRRs; innate immunity; inflammatory disorders;
D O I
10.1007/s00281-007-0081-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The innate immune system relies on a variety of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs) to sense microbial structures that are present in pathogens. Various levels of crosstalk between the TLR and NLR pathways have been described, most notably the description of a molecular scaffold complex, termed the inflammasome, which requires input from both pathways and leads to the activation of the proinflammatory cytokines interleukin (IL)-1 beta and IL-18. In certain cases, the inflammatory process becomes dysregulated and chronic inflammatory diseases may develop. Understanding the interactions of the TLR and NLR pathways will provide further clues to the pathogeneses of these diseases and to the development of efficient therapies to combat them.
引用
收藏
页码:239 / 248
页数:10
相关论文
共 89 条
[1]   ECTODERMAL DYSPLASIA AND IMMUNODEFICIENCY [J].
ABINUN, M .
ARCHIVES OF DISEASE IN CHILDHOOD, 1995, 73 (02) :185-185
[2]   Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections [J].
Agnese, DM ;
Calvano, JE ;
Hahm, SJ ;
Coyle, SM ;
Corbett, SA ;
Calvano, SE ;
Lowry, SF .
JOURNAL OF INFECTIOUS DISEASES, 2002, 186 (10) :1522-1525
[3]   NALP3 forms an IL-lβ-Processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder [J].
Agostini, L ;
Martinon, F ;
Burns, K ;
McDermott, MF ;
Hawkins, PN ;
Tschopp, J .
IMMUNITY, 2004, 20 (03) :319-325
[4]  
Akira S, 2006, CURR TOP MICROBIOL, V311, P1
[5]   Evasion of Toll-like receptor 5 by flagellated bacteria [J].
Andersen-Nissen, E ;
Smith, KD ;
Strobe, KL ;
Barrett, SLR ;
Cookson, BT ;
Logan, SM ;
Aderem, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (26) :9247-9252
[6]   A conserved surface on Toll-like receptor 5 recognizes bacterial flagellin [J].
Andersen-Nissen, Erica ;
Smith, Kelly D. ;
Bonneau, Richard ;
Strong, Roland K. ;
Aderem, Alan .
JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (02) :393-403
[7]   Membrane recruitment of NOD2 in intestinal epithelial cells is essential for nuclear factor-κB activation in muramyl dipeptide recognition [J].
Barnich, N ;
Aguirre, JE ;
Reinecker, HC ;
Xavier, R ;
Podolsky, DK .
JOURNAL OF CELL BIOLOGY, 2005, 170 (01) :21-26
[8]   TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children [J].
Berdeli, A ;
Celik, HA ;
Özyürek, R ;
Dogrusoz, B ;
Aydin, HH .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2005, 83 (07) :535-541
[9]   The interleukin-1 receptor/Toll-like receptor superfamily: signal generators for pro-inflammatory interleukins and microbial products [J].
Bowie, A ;
O'Neill, LAJ .
JOURNAL OF LEUKOCYTE BIOLOGY, 2000, 67 (04) :508-514
[10]   Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin [J].
Boyden, ED ;
Dietrich, WF .
NATURE GENETICS, 2006, 38 (02) :240-244