The inflammasome:: a danger sensing complex triggering innate immunity

被引：578

作者：

Petrilli, Virginie ^{[1
]}

Dostert, Catherine ^{[1
]}

Muruve, Daniel A. ^{[2
]}

Tschopp, Juerg ^{[1
]}

机构：

[1] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland

[2] Univ Calgary, Dept Med, Calgary, AB T2N 1N4, Canada

来源：

CURRENT OPINION IN IMMUNOLOGY | 2007年 / 19卷 / 06期

关键词：

D O I：

10.1016/j.coi.2007.09.002

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 NOD-like receptors (NLR) are a family of intracellular sensors of microbial motifs and 'danger signals' that have emerged as being crucial components of the innate immune responses and inflammation. Several NLRs (NALPs and IPAF) form a caspase-l-activating multiprotein complex, termed inflammasome, that processes proinflammatory cytokines including IL-1 beta. Amongst the various inflammasomes, the NALP3 inflammasome is particularly qualified to sense a plethora of diverse molecules, ranging from bacterial muramyldipeptide to monosodium crate crystals. The important role of the NALP3 inflammasome is emphasized by the identification of mutations in the NALP3 gene that are associated with a susceptibility to inflammatory disorders. These and other issues related to the inflammasome are discussed in this review.

引用

页码：615 / 622

页数：8

共 64 条

[1] 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

[2] Pathogen recognition and innate immunity [J].

Akira, S ;

Uematsu, S ;

Takeuchi, O .

CELL, 2006, 124 (04) :783-801

[3] Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin [J].

Boyden, ED ;

Dietrich, WF .

NATURE GENETICS, 2006, 38 (02) :240-244

[4] Bcl-2 and Bcl-XL regulate proinf lammatory caspase-1 activation by interaction with NALP1 [J].

Bruey, Jean-Marie ;

Bruey-Sedano, Nathalie ;

Luciano, Frederic ;

Zhai, Dayong ;

Balpai, Ruchi ;

Xu, Chunyan ;

Kress, Christina L. ;

Bailly-Maitre, Beatrice ;

Li, Xiaoqing ;

Osterman, Andrei ;

Matsuzawa, Shu-ichi ;

Terskikh, Alexey V. ;

Faustin, Benjamin ;

Reed, John C. .

CELL, 2007, 129 (01) :45-56

[5] The systemic autoinflammatory diseases: Inborn errors of the innate immune system [J].

Brydges, S. ;

Kastner, D. L. .

CURRENT CONCEPTS IN AUTOIMMUNITY AND CHRONIC INFLAMATION, 2006, 305 :127-160

[6] Maturation and release of interleukin-1β by lipopolysaccharide-primed mouse Schwann cells require the stimulation of P2X7 receptors [J].

Colomar, A ;

Marty, V ;

Médina, C ;

Combe, C ;

Parnet, P ;

Amédée, T .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (33) :30732-30740

[7] SGT1 is essential for Nod1 activation [J].

Correia, Jean da Silva ;

Miranda, Yvonne ;

Leonard, Nikki ;

Ulevitch, Richard .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (16) :6764-6769

[8] ATP activates a reactive oxygen species-dependent oxidative stress response and secretion of proinflammatory cytokines in macrophages [J].

Cruz, Cristiane M. ;

Rinna, Alessandra ;

Forman, Henry Jay ;

Ventura, Ana L. M. ;

Persechini, Pedro M. ;

Ojcius, David M. .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (05) :2871-2879

[9] Birc1e is the gene within the Lgn1 locus associated with resistance to Legionella pneumophila [J].

Diez, E ;

Lee, SH ;

Gauthier, S ;

Yaraghi, Z ;

Tremblay, M ;

Vidal, S ;

Gros, P .

NATURE GENETICS, 2003, 33 (01) :55-60

[10] Interleukin-1β, interleukin-18, and the interleukin-1β converting enzyme [J].

Dinarello, CA .

MOLECULAR MECHANISMS OF FEVER, 1998, 856 :1-11

← 1 2 3 4 5 6 7 →