The inflammasomes in health and disease: from genetics to molecular mechanisms of autoinflammation and beyond

被引：88

作者：

Conforti-Andreoni, Cristina ^{[1
]}

Ricciardi-Castagnoli, Paola ^{[1
]}

Mortellaro, Alessandra ^{[1
]}

机构：

[1] ASTAR, Singapore Immunol Network, Singapore 138648, Singapore

来源：

CELLULAR & MOLECULAR IMMUNOLOGY | 2011年 / 8卷 / 02期

关键词：

autoinflammatory diseases; polymorphisms; NLRs; NLRP3; MULTISYSTEM INFLAMMATORY DISEASE; PATTERN-RECOGNITION RECEPTORS; INNATE IMMUNE-RESPONSES; LOW-LEVEL MOSAICISM; KAPPA-B ACTIVATION; NOD-LIKE RECEPTORS; NALP3; INFLAMMASOME; NLRP3; T-CELLS; CASPASE-1; ACTIVATION;

D O I：

10.1038/cmi.2010.81

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Nucleotide-binding oligomerization domain (NOD)-containing protein-like receptors (NLRs) are a recently discovered class of innate immune receptors that play a crucial role in initiating the inflammatory response following pathogen recognition. Some NLRs form the framework for cytosolic platforms called inflammasomes, which orchestrate the early inflammatory process via IL-1 beta activation. Mutations and polymorphisms in NLR-coding genes or in genetic loci encoding inflammasome-related proteins correlate with a variety of autoinflammatory diseases. Moreover, the activity of certain inflammasomes is associated with susceptibility to infections as well as autoimmunity and tumorigenesis. In this review, we will discuss how identifying the genetic characteristics of inflammasomes is assisting our understanding of both autoinflammatory diseases as well as other immune system-driven disorders. Cellular & Molecular Immunology (2011) 8, 135-145; doi:10.1038/cmi.2010.81; published online 24 January 2011

引用

页码：135 / 145

页数：11

共 138 条

[1] Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells [J].

Acosta-Rodriguez, Eva V. ;

Napolitani, Giorgio ;

Lanzavecchia, Antonio ;

Sallusto, Federica .

NATURE IMMUNOLOGY, 2007, 8 (09) :942-949

[2] Association of mutations in the NALP3/CIAS1/PYPAF1 gene with a broad phenotype including recurrent fever, cold sensitivity, sensorineural deafness, and AA amyloidosis [J].

Aganna, E ;

Martinon, F ;

Hawkins, PN ;

Ross, JB ;

Swan, DC ;

Booth, DR ;

Lachmann, HJ ;

Gaudet, R ;

Woo, P ;

Feighery, C ;

Cotter, FE ;

Thome, M ;

Hitman, GA ;

Tschopp, J ;

McDermott, MF .

ARTHRITIS AND RHEUMATISM, 2002, 46 (09) :2445-2452

[3]

Agarwal S, 2008, J RHEUMATOL, V35, P515

[4] De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID) -: A new member of the expanding family of pyrin-associated autoinflammatory diseases [J].

Aksentijevich, I ;

Nowak, M ;

Mallah, M ;

Chae, JJ ;

Watford, WT ;

Hofmann, SR ;

Stein, L ;

Russo, R ;

Goldsmith, D ;

Dent, P ;

Rosenberg, HF ;

Austin, F ;

Remmers, EF ;

Balow, JE ;

Rosenzweig, S ;

Komarow, H ;

Shoham, NG ;

Wood, G ;

Jones, J ;

Mangra, N ;

Carrero, H ;

Adams, BS ;

Moore, TL ;

Schikler, K ;

Hoffman, H ;

Lovell, DJ ;

Lipnick, R ;

Barron, K ;

O'Shea, JJ ;

Kastner, DL ;

Goldbach-Mansky, R .

ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3340-3348

[5] Mutational analysis in neonatal-onset multisystem innammatory disease: comment on the articles by Frenkel et al and Saito et al [J].

Aksentijevich, Ivona ;

Remmers, Elaine F. ;

Goldbach-Mansky, Raphaela ;

Reiff, Andreas ;

Kastner, Daniel L. .

ARTHRITIS AND RHEUMATISM, 2006, 54 (08) :2703-2704

[6] The NLRP3 inflammasome functions as a negative regulator of tumorigenesis during colitis-associated cancer [J].

Allen, Irving C. ;

TeKippe, Erin McElvania ;

Woodford, Rita-Marie T. ;

Uronis, Joshua M. ;

Holl, Eda K. ;

Rogers, Arlin B. ;

Herfarth, Hans H. ;

Jobin, Christian ;

Ting, Jenny P. -Y. .

JOURNAL OF EXPERIMENTAL MEDICINE, 2010, 207 (05) :1045-1056

[7] The NLRP3 Inflammasome Mediates In Vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA [J].

Allen, Irving C. ;

Scull, Margaret A. ;

Moore, Chris B. ;

Holl, Eda K. ;

McElvania-TeKippe, Erin ;

Taxman, Debra J. ;

Guthrie, Elizabeth H. ;

Pickles, Raymond J. ;

Ting, Jenny P. -Y. .

IMMUNITY, 2009, 30 (04) :556-565

[8] A Somatic NLRP3 Mutation as a Cause of a Sporadic Case of Chronic Infantile Neurologic, Cutaneous, Articular Syndrome/Neonatal-Onset Multisystem Inflammatory Disease Novel Evidence of the Role of Low-Level Mosaicism as the Pathophysiologic Mechanism Underlying Mendelian Inherited Diseases [J].

Arostegui, Juan I. ;

Lopez Saldana, Ma Dolores ;

Pascal, Mariona ;

Clemente, Daniel ;

Aymerich, Marta ;

Balaguer, Francesc ;

Goel, Ajay ;

Fournier del Castillo, Concepcion ;

Rius, Josefa ;

Plaza, Susana ;

Lopez Robledillo, Juan Carlos ;

Juan, Manel ;

Ibanez, Mercedes ;

Yaguee, Jordi .

ARTHRITIS AND RHEUMATISM, 2010, 62 (04) :1158-1166

[9] Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression [J].

Bauernfeind, Franz G. ;

Horvath, Gabor ;

Stutz, Andrea ;

Alnemri, Emad S. ;

MacDonald, Kelly ;

Speert, David ;

Fernandes-Alnemri, Teresa ;

Wu, Jianghong ;

Monks, Brian G. ;

Fitzgerald, Katherine A. ;

Hornung, Veit ;

Latz, Eicke .

JOURNAL OF IMMUNOLOGY, 2009, 183 (02) :787-791

[10] The leucine-rich repeat structure [J].

Bella, J. ;

Hindle, K. L. ;

McEwan, P. A. ;

Lovell, S. C. .

CELLULAR AND MOLECULAR LIFE SCIENCES, 2008, 65 (15) :2307-2333

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