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• W1498781671 abstract "Two of the main challenges that eukaryotic multicellular organisms faced during evolution were to cope with invading microorganisms and to eliminate infected cells. The immune system evolved to handle both tasks. Intertwined with immunity is programmed cell death that tailors the immune response and provides an effective way to remove infected cells. Caspases, effectors of inflammation and programmed cell death cascades, are perfectly suited to regulate the host response to invaders and injury. Their activity as inflammatory and killer proteases is regulated by direct binding to sensors of pathogens or danger, they can be modified following activation of signalling cascades by feedback mechanisms to terminate the inflammatory response and control cell survival, and they associate with coactivators and corepressors whose expression is closely linked to the needs of the cell.Key concepts Cell death and innate immunity are ancient evolutionarily conserved processes that utilize a number of related effectors and parallel signal transduction mechanisms.Innate immunity provides first line defences against pathogens and acts as a sentinel that primes adaptive immunity.Innate immunity depends on evolutionarily conserved germline-encoded pattern recognition receptors (PRRs) that ‘sense’ pathogen-associated molecular patterns (PAMPs) and ‘danger’ signals.The role of caspases in innate immunity is conserved through evolution.Caspase-1, the prototypical member of the inflammatory caspase subfamily, contributes to host defence through different interrelated mechanisms, notably cell repair, inflammation and cell death.Caspase-1 activity is necessary for host resistance to pathogens; however, when deregulated, it is at the basis of multiple inflammatory diseases.Inflammatory caspases are activated in NLR-scaffolded multiprotein complexes termed ‘inflammasomes’ that are reminiscent of the apoptosome. Caspase-12, an inflammatory caspase related to caspase-1, is an endogenous inhibitor of the inflammasome.Apoptosis tailors adaptive immunity. Mutations in Casp-8 and Casp-10 cause autoimmune lymphoproliferative syndrome (ALPS).Excessive apoptotic caspase activity contributes to the pathogenesis of inflammatory diseases such as severe sepsis.Keywords:caspases;inflammation;immunity;pattern recognition receptors;inflammatory and autoimmune diseases" @default.
• W1498781671 created "2016-06-24" @default.
• W1498781671 creator A5017363021 @default.
• W1498781671 creator A5054270478 @default.
• W1498781671 date "2009-09-15" @default.
• W1498781671 modified "2023-09-26" @default.
• W1498781671 title "Caspases in Inflammation and Immunity" @default.
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• W1498781671 doi "https://doi.org/10.1002/9780470015902.a0021990" @default.
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