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10.1016/j.mib.2013.04.004

http://scihub22266oqcxt.onion/10.1016/j.mib.2013.04.004
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C3742712!3742712!23707339
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suck abstract from ncbi


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pmid23707339      Curr+Opin+Microbiol 2013 ; 16 (3): 319-26
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  • Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection #MMPMID23707339
  • Aachoui Y; Sagulenko V; Miao EA; Stacey KJ
  • Curr Opin Microbiol 2013[Jun]; 16 (3): 319-26 PMID23707339show ga
  • Cell death is an effective strategy to limit intracellular infections. Canonical inflammasomes, including NLRP3, NLRC4, and AIM2, recruit and activate caspase-1 in response to a range of microbial stimuli and endogenous danger signals. Caspase-1 then promotes the secretion of IL-1? and IL-18 and a rapid form of lytic programmed cell death termed pyroptosis. A second inflammatory caspase, mouse caspase-11, mediates pyroptotic death through an unknown non-canonical inflammasome system in response to cytosolic bacteria. In addition, recent work shows that inflammasomes can also recruit procaspase-8, initiating apoptosis. The induction of multiple pathways of cell death has probably evolved to counteract microbial evasion of cell death pathways.
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