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Cell Mol Life Sci
2010 May 01;6710:1643-51. doi: 10.1007/s00018-010-0335-5.
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Control of infection by pyroptosis and autophagy: role of TLR and NLR.
Bortoluci KR
,
Medzhitov R
.
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Cells can die by distinct mechanisms with particular impacts on the immune response. In addition to apoptosis and necrosis, recent studies lead to characterization of a new pro-inflammatory form of cell death, pyroptosis. TLR and NLR, central innate immune sensors, can control infections by modulating host cell survival. In addition, TLRs can promote the induction of autophagy, thus promoting delivery of infecting pathogens to the lysosomes. On the other hand, activation of some NLR members, especially NLRC4 and NAIP5, leads to the infected cell death by pyroptosis, which is accompanied by secretion of the pro-inflammatory cytokines IL-1beta, IL-18, and IL-33. Data presented here illustrate how the compartmentalization of the innate immune sensors can influence the outcome of infections by controlling the fate of host cells.
Akhter,
Caspase-7 activation by the Nlrc4/Ipaf inflammasome restricts Legionella pneumophila infection.
2009, Pubmed
Akhter,
Caspase-7 activation by the Nlrc4/Ipaf inflammasome restricts Legionella pneumophila infection.
2009,
Pubmed
Akira,
Toll-like receptor signalling.
2004,
Pubmed
Amer,
Regulation of Legionella phagosome maturation and infection through flagellin and host Ipaf.
2006,
Pubmed
Amer,
Autophagy is an immediate macrophage response to Legionella pneumophila.
2005,
Pubmed
Andrade,
CD40 induces macrophage anti-Toxoplasma gondii activity by triggering autophagy-dependent fusion of pathogen-containing vacuoles and lysosomes.
2006,
Pubmed
Bergsbaken,
Pyroptosis: host cell death and inflammation.
2009,
Pubmed
Bergsbaken,
Macrophage activation redirects yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis.
2007,
Pubmed
Birmingham,
Autophagy controls Salmonella infection in response to damage to the Salmonella-containing vacuole.
2006,
Pubmed
Boyden,
Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin.
2006,
Pubmed
Carty,
The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling.
2006,
Pubmed
Checroun,
Autophagy-mediated reentry of Francisella tularensis into the endocytic compartment after cytoplasmic replication.
2006,
Pubmed
Degterev,
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury.
2005,
Pubmed
Delgado,
Toll-like receptors control autophagy.
2008,
Pubmed
Dostert,
Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica.
2008,
Pubmed
Dostert,
Malarial hemozoin is a Nalp3 inflammasome activating danger signal.
2009,
Pubmed
Franchi,
Critical role for Ipaf in Pseudomonas aeruginosa-induced caspase-1 activation.
2007,
Pubmed
Franchi,
Cytosolic flagellin requires Ipaf for activation of caspase-1 and interleukin 1beta in salmonella-infected macrophages.
2006,
Pubmed
Franchi,
The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis.
2009,
Pubmed
Franchi,
Differential requirement of P2X7 receptor and intracellular K+ for caspase-1 activation induced by intracellular and extracellular bacteria.
2007,
Pubmed
Franchi,
Function of Nod-like receptors in microbial recognition and host defense.
2009,
Pubmed
Grimm,
RIP and FADD: two "death domain"-containing proteins can induce apoptosis by convergent, but dissociable, pathways.
1996,
Pubmed
Gross,
Syk kinase signalling couples to the Nlrp3 inflammasome for anti-fungal host defence.
2009,
Pubmed
Gutierrez,
Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages.
2004,
Pubmed
Hernandez,
A Salmonella protein causes macrophage cell death by inducing autophagy.
2003,
Pubmed
Holler,
Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule.
2000,
Pubmed
Inohara,
Nod1, an Apaf-1-like activator of caspase-9 and nuclear factor-kappaB.
1999,
Pubmed
Joly,
Cutting edge: Candida albicans hyphae formation triggers activation of the Nlrp3 inflammasome.
2009,
Pubmed
Kang,
Bacillus anthracis spores and lethal toxin induce IL-1beta via functionally distinct signaling pathways.
2008,
Pubmed
Kanneganti,
Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3.
2006,
Pubmed
Kanneganti,
Intracellular NOD-like receptors in host defense and disease.
2007,
Pubmed
Kanneganti,
Critical role for Cryopyrin/Nalp3 in activation of caspase-1 in response to viral infection and double-stranded RNA.
2006,
Pubmed
Kawai,
TLR signaling.
2007,
Pubmed
Kroemer,
Autophagic cell death: the story of a misnomer.
2008,
Pubmed
Lamkanfi,
Fungal zymosan and mannan activate the cryopyrin inflammasome.
2009,
Pubmed
Lightfield,
Critical function for Naip5 in inflammasome activation by a conserved carboxy-terminal domain of flagellin.
2008,
Pubmed
Ling,
Vacuolar and plasma membrane stripping and autophagic elimination of Toxoplasma gondii in primed effector macrophages.
2006,
Pubmed
Mariathasan,
Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf.
2004,
Pubmed
Mariathasan,
Cryopyrin activates the inflammasome in response to toxins and ATP.
2006,
Pubmed
Marina-García,
Pannexin-1-mediated intracellular delivery of muramyl dipeptide induces caspase-1 activation via cryopyrin/NLRP3 independently of Nod2.
2008,
Pubmed
Martinon,
The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.
2002,
Pubmed
Martinon,
Identification of bacterial muramyl dipeptide as activator of the NALP3/cryopyrin inflammasome.
2004,
Pubmed
Martinon,
Gout-associated uric acid crystals activate the NALP3 inflammasome.
2006,
Pubmed
Martinon,
Inflammatory caspases and inflammasomes: master switches of inflammation.
2007,
Pubmed
Miao,
Cytoplasmic flagellin activates caspase-1 and secretion of interleukin 1beta via Ipaf.
2006,
Pubmed
Muruve,
The inflammasome recognizes cytosolic microbial and host DNA and triggers an innate immune response.
2008,
Pubmed
Nour,
Anthrax lethal toxin triggers the formation of a membrane-associated inflammasome complex in murine macrophages.
2009,
Pubmed
Ogura,
Nod2, a Nod1/Apaf-1 family member that is restricted to monocytes and activates NF-kappaB.
2001,
Pubmed
Palm,
Pattern recognition receptors and control of adaptive immunity.
2009,
Pubmed
Poyet,
Identification of Ipaf, a human caspase-1-activating protein related to Apaf-1.
2001,
Pubmed
Py,
Autophagy limits Listeria monocytogenes intracellular growth in the early phase of primary infection.
2007,
Pubmed
Saitoh,
Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1beta production.
2008,
Pubmed
Sanjuan,
Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis.
2007,
Pubmed
Sanjuan,
Toll-like receptor signaling in the lysosomal pathways.
2009,
Pubmed
Shi,
MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages.
2008,
Pubmed
Shio,
Malarial hemozoin activates the NLRP3 inflammasome through Lyn and Syk kinases.
2009,
Pubmed
Sutterwala,
Critical role for NALP3/CIAS1/Cryopyrin in innate and adaptive immunity through its regulation of caspase-1.
2006,
Pubmed
Sutterwala,
Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome.
2007,
Pubmed
Suzuki,
Differential regulation of caspase-1 activation, pyroptosis, and autophagy via Ipaf and ASC in Shigella-infected macrophages.
2007,
Pubmed
Ting,
NLRs at the intersection of cell death and immunity.
2008,
Pubmed
Warren,
Multiple Nod-like receptors activate caspase 1 during Listeria monocytogenes infection.
2008,
Pubmed
Zamboni,
The Birc1e cytosolic pattern-recognition receptor contributes to the detection and control of Legionella pneumophila infection.
2006,
Pubmed
