Emerging concepts about NAIP/NLIRC4 inflammasomes

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dc.contributor.authorLage, Silvia Lucena [UNIFESP]
dc.contributor.authorLongo, Carla [UNIFESP]
dc.contributor.authorBranco, Laura Migliari [UNIFESP]
dc.contributor.authorCosta, Thais Boccia da [UNIFESP]
dc.contributor.authorBuzzo, Carina de Lima [UNIFESP]
dc.contributor.authorBortoluci, Karina Ramalho [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:37:35Z
dc.date.available2016-01-24T14:37:35Z
dc.date.issued2014-07-02
dc.description.abstractNeuronal apoptosis inhibitory protein (NAIP)/NOD-like receptor (NLR) containing a caspase activating and recruitment domain (CARD) 4 (NLRC4) inflammasome complexes are activated in response to proteins from virulent bacteria that reach the cell cytosol. Specific NAIP proteins bind to the agonists and then physically associate with NLRC4 to form an inflammasome complex able to recruit and activate pro-caspase-1. NAIP5 and NAIP6 sense flagellin, component of flagella from motile bacteria, whereas NAIP1 and NAIP2 detect needle and rod components from bacterial type III secretion systems, respectively. Active caspase-1 mediates the maturation and secretion of the pro-inflammatory cytokines, 11,113 and 11,18, and is responsible for the induction of pyroptosis, a pro-inflammatory form of cell death. in addition to these well-known effector mechanisms, novel roles have been described for NAIP/NLRC4 inflammasomes, such as phagosomal maturation, activation of inducible nitric oxide synthase, regulation of autophagy, secretion of inflammatory mediators, antibody production, activation of T cells, among others. These effector mechanisms mediated by NAIP/NLRC4 inflammasomes have been extensively studied in the context of resistance of infections and the potential of their agonists has been exploited in therapeutic strategies to non-infectious pathologies, such as tumor protection. Thus, this review will discuss current knowledge about the activation of NAIP/NLRC4 inflammasomes and their effector mechanisms.en
dc.description.affiliationUniversidade Federal de São Paulo, Ctr Terapia Celulare & Mol CTC Mol, BR-04044010 São Paulo, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04044010 São Paulo, SP, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Ctr Terapia Celulare & Mol CTC Mol, BR-04044010 São Paulo, SP, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04044010 São Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipINCTV
dc.description.sponsorshipIDFAPESP: 2013/16010-5
dc.format.extent10
dc.identifierhttp://dx.doi.org/10.3389/fimmu.2014.00309
dc.identifier.citationFrontiers in Immunology. Lausanne: Frontiers Research Foundation, v. 5, 10 p., 2014.
dc.identifier.doi10.3389/fimmu.2014.00309
dc.identifier.fileWOS000354374800001.pdf
dc.identifier.issn1664-3224
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/37983
dc.identifier.wosWOS:000354374800001
dc.language.isoeng
dc.publisherFrontiers Research Foundation
dc.relation.ispartofFrontiers in Immunology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNAIPen
dc.subjectNLRC4en
dc.subjectflagellinen
dc.subjectcaspase-1en
dc.subjectinflammasomesen
dc.subjectlysosomesen
dc.subjectcell deathen
dc.titleEmerging concepts about NAIP/NLIRC4 inflammasomesen
dc.typeinfo:eu-repo/semantics/article
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