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dc.contributor.authorAwad, Fawaz
dc.contributor.authorAssrawi, Eman
dc.contributor.authorLouvrier, Camille
dc.contributor.authorJumeau, Claire
dc.contributor.authorGeorgin-Lavialle, Sophie
dc.contributor.authorGrateau, Gilles
dc.contributor.authorAmselem, Serge
dc.contributor.authorGiurgea, Irina
dc.contributor.authorKarabina, Sonia-Athina
dc.date.accessioned2019-12-18T12:27:51Z
dc.date.available2019-12-18T12:27:51Z
dc.date.issued2018-02-18
dc.identifier.issn0163-7258
dc.identifier.urihttps://dspace.alquds.edu/handle/20.500.12213/5046
dc.description.abstractInflammasomes are intracellular multiprotein signaling complexes, mainly present in myeloid cells. They commonly assemble around a cytoplasmic receptor of the nucleotide-binding leucine-rich repeat containing receptor (NLR) family, although other cytoplasmic receptors like pyrin have been shown to forminflammasomes. The nucleation of the multiprotein scaffolding platform occurs upon detection of a microbial, a danger or a homeostasis pattern by the receptor that will, most commonly, associate with the adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD) through homotypic domain interactions resulting in recruitment of procaspase-1. This will lead to the autoproteolytic activation of caspase-1, which regulates the secretion of proinflammatory IL1β and IL18 cytokines and pyroptosis, a caspase-1-mediated form of cell death. Pyroptosis occurs through cleavage of Gasdermin D, a membrane pore forming protein. Recently, non-canonical inflammasomes have been described, which directly sense intracellular pathogens through caspase-4 and -5 in humans, leading to pyroptosis. Inflammasomes are important in host defense; however, a deregulated activity is associated with a number of inflammatory, immune and metabolic disorders. Furthermore, mutations in inflammasome receptor coding genes are causal for an increasing number of rare autoinflammatory diseases. Biotherapies targeting the products of inflammasome activation aswell as molecules that directly or indirectly inhibit inflammasome nucleation and activation are promising therapeutic areas. This review discusses recent advances in inflammasome biology, the molecular pathology of several inflammasomes, and current therapeutic approaches in autoinflammatory diseases and in selected common multifactorial inflammasome-mediated disorders.en_US
dc.language.isoenen_US
dc.publisherElsevier Inc.en_US
dc.subjectAutoinflammationen_US
dc.subjectInflammasomesen_US
dc.subjectPyrinen_US
dc.subjectPyroptosisen_US
dc.subjectCytokinesen_US
dc.titleInflammasome biology, molecular pathology and therapeutic implicationsen_US
dc.typeArticleen_US


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