NOD-Like Receptors: Role in Innate Immunity and Inflammatory Disease

被引:588
作者
Chen, Grace [1 ]
Shaw, Michael H.
Kim, Yun-Gi
Nunez, Gabriel
机构
[1] Univ Michigan, Dept Pathol, Ctr Comprehens Canc, Sch Med, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
caspase-1; Crohns disease; IL-1; NOD2; NLRP3; NF-KAPPA-B; TOLL-LIKE-RECEPTOR; FAMILIAL MEDITERRANEAN FEVER; INTESTINAL EPITHELIAL-CELLS; LEGIONELLA-PNEUMOPHILA INFECTION; COLD AUTOINFLAMMATORY SYNDROME; BACTERIAL MURAMYL DIPEPTIDE; INVASIVE SHIGELLA-FLEXNERI; ALPHA-DEFENSIN EXPRESSION; BARE LYMPHOCYTE SYNDROME;
D O I
10.1146/annurev.pathol.4.110807.092239
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The NOD-like receptors (NLRs) are a specialized group of intracellular receptors that represent a key component of the host innate immune system. Since the discovery of the first NLR almost 10 years ago, the study of this special class of microbial sensors has burgeoned; consequently, a better understanding of the mechanism by which these receptors recognize microbes and other danger signals and of how they activate inflammatory signaling pathways, has emerged. Moreover, in addition to their primary role in host defense against invading pathogens, their ability to regulate nuclear factor-kappa B (NF-kappa B) signaling, interleukin-1-beta (IL-1 beta) production, and cell death indicates that they are crucial to the pathogenesis of a variety of inflammatory human diseases.
引用
收藏
页码:365 / 398
页数:34
相关论文
共 174 条
[1]   Coordinated regulation of toll-like receptor and NOD2 signaling by k63-linked polyubiquitin chains [J].
Abbott, Derek W. ;
Yang, Yibin ;
Hutti, Jessica E. ;
Madhavarapu, Swetha ;
Kelliher, Michelle A. ;
Cantley, Lewis C. .
MOLECULAR AND CELLULAR BIOLOGY, 2007, 27 (17) :6012-6025
[2]   The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO [J].
Abbott, DW ;
Wilkins, A ;
Asara, JM ;
Cantley, LC .
CURRENT BIOLOGY, 2004, 14 (24) :2217-2227
[3]   TLR signaling at the intestinal epithelial interface [J].
Abreu, MT ;
Thomas, LS ;
Arnold, ET ;
Lukasek, K ;
Michelsen, KS ;
Arditi, M .
JOURNAL OF ENDOTOXIN RESEARCH, 2003, 9 (05) :322-330
[4]   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
[5]   Regulation of Legionella phagosome maturation and infection through flagellin and host Ipaf [J].
Amer, Amal ;
Franchi, Luigi ;
Kanneganti, Thirumala-Devi ;
Body-Malapel, Mathilde ;
Ozoren, Nesrin ;
Brady, Graham ;
Meshinchi, Sasha ;
Jagirdar, Rajesh ;
Gewirtz, Andrew ;
Akira, Shizuo ;
Nunez, Gabriel .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (46) :35217-35223
[6]   Autophagy is an immediate macrophage response to Legionella pneumophila [J].
Amer, AO ;
Swanson, MS .
CELLULAR MICROBIOLOGY, 2005, 7 (06) :765-778
[7]   Siblings, day-care attendance, and the risk of asthma and wheezing during childhood [J].
Ball, TM ;
Castro-Rodriguez, JA ;
Griffith, KA ;
Holberg, CJ ;
Martinez, FD ;
Wright, AL .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (08) :538-543
[8]   Macrophage activation redirects Yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis [J].
Bergsbaken, Tessa ;
Cookson, Brad T. .
PLOS PATHOGENS, 2007, 3 (11) :1570-1582
[9]   FAMILIAL GRANULOMATOUS ARTHRITIS, IRITIS, AND RASH [J].
BLAU, EB .
JOURNAL OF PEDIATRICS, 1985, 107 (05) :689-693
[10]   Neonatal-onset multisystem inflammatory disease (NOMID) due to a novel S331R mutation of the CIAS1 gene and response to interleukin-1 receptor antagonist treatment [J].
Boschan, C ;
Witt, O ;
Lohse, P ;
Foeldvari, I ;
Zappel, H ;
Schweigerer, L .
AMERICAN JOURNAL OF MEDICAL GENETICS PART A, 2006, 140A (08) :883-886