Inflammasomes

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  Subject Areas on Research

  • A CRISPR-Cas system enhances envelope integrity mediating antibiotic resistance and inflammasome evasion. 
  • A licence to kill during inflammation. 
  • A noncanonical function of cGAMP in inflammasome priming and activation. 
  • A possible mechanism underlying mood disorders associated with LUTS: Chronic bladder outlet obstruction causes NLRP3-dependent inflammation in the hippocampus and depressive behavior in rats. 
  • A tumor-intrinsic PD-L1/NLRP3 inflammasome signaling pathway drives resistance to anti-PD-1 immunotherapy. 
  • Activation of the NLRP3 inflammasome by intracellular poly I:C. 
  • Activation of the Nlrp3 inflammasome by mitochondrial reactive oxygen species: a novel mechanism of albumin-induced tubulointerstitial inflammation. 
  • An NLRP3 Mutation Causes Arthropathy and Osteoporosis in Humanized Mice. 
  • An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage. 
  • Annexin-A1 Tripeptide Attenuates Surgery-Induced Neuroinflammation and Memory Deficits Through Regulation the NLRP3 Inflammasome. 
  • Application of immobilized ATP to the study of NLRP inflammasomes. 
  • Autophagy links inflammasomes to atherosclerotic progression. 
  • Bisphosphonates target B cells to enhance humoral immune responses. 
  • Bladder fibrosis during outlet obstruction is triggered through the NLRP3 inflammasome and the production of IL-1β. 
  • Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4. 
  • Canonical Inflammasomes Drive IFN-γ to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium. 
  • Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria. 
  • Caspase-1-induced pyroptotic cell death. 
  • Caspase-11 interaction with NLRP3 potentiates the noncanonical activation of the NLRP3 inflammasome. 
  • Caspase-11 protects against bacteria that escape the vacuole. 
  • Damage-Associated Molecular Patterns Induce Inflammatory Injury During Machine Preservation of the Liver: Potential Targets to Enhance a Promising Technology. 
  • Detection of cytosolic bacteria by inflammatory caspases. 
  • Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity. 
  • Diabetic bladder dysfunction progresses from an overactive to an underactive phenotype in a type-1 diabetic mouse model (Akita female mouse) and is dependent on NLRP3. 
  • Differential requirements for NAIP5 in activation of the NLRC4 inflammasome. 
  • Down with doublespeak: NAIP/NLRC4 inflammasomes get specific. 
  • Dynamin-related Irgm proteins modulate LPS-induced caspase-11 activation and septic shock. 
  • Elevated hydrostatic pressure stimulates ATP release which mediates activation of the NLRP3 inflammasome via P2X4 in rat urothelial cells. 
  • Environmental Factors Modify the Severity of Acute DSS Colitis in Caspase-11-Deficient Mice. 
  • Frontline Science: Multiple cathepsins promote inflammasome-independent, particle-induced cell death during NLRP3-dependent IL-1β activation. 
  • Gasdermins: Effectors of Pyroptosis. 
  • Guanylate Binding Proteins Regulate Inflammasome Activation in Response to Hyperinjected Yersinia Translocon Components. 
  • Guanylate binding proteins enable rapid activation of canonical and noncanonical inflammasomes in Chlamydia-infected macrophages. 
  • HIV vaccine candidate activation of hypoxia and the inflammasome in CD14+ monocytes is associated with a decreased risk of SIVmac251 acquisition. 
  • Holding the Inflammatory System in Check: TLRs and NLRs. 
  • Human guanylate binding proteins: nanomachines orchestrating host defense. 
  • Hydroxychloroquine attenuates renal ischemia/reperfusion injury by inhibiting cathepsin mediated NLRP3 inflammasome activation. 
  • IKKα negatively regulates ASC-dependent inflammasome activation. 
  • IL-1β, IL-18, and eicosanoids promote neutrophil recruitment to pore-induced intracellular traps following pyroptosis. 
  • Immune activation by histones: plusses and minuses in inflammation. 
  • Immunological Aspects of Age-Related Macular Degeneration. 
  • Inflammasome Activation by Bacterial Outer Membrane Vesicles Requires Guanylate Binding Proteins. 
  • Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). 
  • Inflammasome expression and cytomegalovirus viremia in critically ill patients with sepsis. 
  • Inflammasome signaling in human placental trophoblasts regulates immune defense against Listeria monocytogenes infection. 
  • Inflammasome, Inflammation, and Tissue Homeostasis. 
  • Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection. 
  • Inflammasomes Coordinate Pyroptosis and Natural Killer Cell Cytotoxicity to Clear Infection by a Ubiquitous Environmental Bacterium. 
  • Inflammasomes are important mediators of cyclophosphamide-induced bladder inflammation. 
  • Inflammasomes in the urinary tract: a disease-based review. 
  • Inhibition of Human Dendritic Cell ER Stress Response Reduces T Cell Alloreactivity Yet Spares Donor Anti-tumor Immunity. 
  • Innate Immune Activation in High-risk Donor Kidneys: An Opportunity to Intervene? 
  • Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection. 
  • Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome. 
  • Investigating the Role of Inflammasome Caspases 1 and 11 in the Acute Radiation Syndrome. 
  • LPS-aggregating proteins GBP1 and GBP2 are each sufficient to enhance caspase-4 activation both in cellulo and in vitro. 
  • MCC950, a selective NLPR3 inflammasome inhibitor, improves neurologic function and survival after cardiac arrest and resuscitation. 
  • Mechanisms of NOD-like receptor-associated inflammasome activation. 
  • Megalin/Cubulin-Lysosome-mediated Albumin Reabsorption Is Involved in the Tubular Cell Activation of NLRP3 Inflammasome and Tubulointerstitial Inflammation. 
  • Mitochondrial DNA, oxidants, and innate immunity. 
  • Mitochondrial Oxidative Phosphorylation Complex Regulates NLRP3 Inflammasome Activation and Predicts Patient Survival in Nasopharyngeal Carcinoma. 
  • Mitochondrial Quality Control as a Therapeutic Target. 
  • Mitochondrial ROS and NLRP3 inflammasome in acute ozone-induced murine model of airway inflammation and bronchial hyperresponsiveness. 
  • NAIP inflammasomes give the NOD to bacterial ligands. 
  • NLRP1 - One NLR to guard them all. 
  • NLRP3/IL-1β mediates denervation during bladder outlet obstruction in rats. 
  • Naïve CD8 T cell IFNγ responses to a vacuolar antigen are regulated by an inflammasome-independent NLRP3 pathway and Toxoplasma gondii ROP5. 
  • Necroptosis-independent signaling by the RIP kinases in inflammation. 
  • Necrosis-dependent and independent signaling of the RIP kinases in inflammation. 
  • Neutrophil Caspase-11 Is Essential to Defend against a Cytosol-Invasive Bacterium. 
  • Neutrophil inflammasomes sense the subcellular delivery route of translocated bacterial effectors and toxins. 
  • Olfactory receptor 2 in vascular macrophages drives atherosclerosis by NLRP3-dependent IL-1 production. 
  • Olfactory receptors in macrophages and inflammation. 
  • Participation of c-FLIP in NLRP3 and AIM2 inflammasome activation. 
  • Potentiation of P2RX7 as a host-directed strategy for control of mycobacterial infection. 
  • Programmed necrosis in the cross talk of cell death and inflammation. 
  • Pyroptotic cell death defends against intracellular pathogens. 
  • Pyruvate dehydrogenase kinase supports macrophage NLRP3 inflammasome activation during acute inflammation. 
  • Re-Examination of the Exacerbating Effect of Inflammasome Components during Radiation Injury. 
  • Reassessing the Evolutionary Importance of Inflammasomes. 
  • Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis. 
  • Shigella IpaH9.8 limits GBP1-dependent LPS release from intracytosolic bacteria to suppress caspase-4 activation. 
  • Targeting Inflammasomes to Treat Neurological Diseases. 
  • The AIM2 inflammasome is activated in astrocytes during the late phase of EAE. 
  • The Crohn's Disease Risk Factor IRGM Limits NLRP3 Inflammasome Activation by Impeding Its Assembly and by Mediating Its Selective Autophagy. 
  • The Mitochondrial Phosphatase PGAM5 Is Dispensable for Necroptosis but Promotes Inflammasome Activation in Macrophages. 
  • The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction. 
  • The NLRP3 inflammasome detects encephalomyocarditis virus and vesicular stomatitis virus infection. 
  • The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation. 
  • The RIP1-RIP3 complex initiates mitochondrial fission to fuel NLRP3. 
  • The Role of Cell Death in the Pathogenesis of SLE: Is Pyroptosis the Missing Link? 
  • The pathological role of NLRs and AIM2 inflammasome-mediated pyroptosis in damaged blood-brain barrier after traumatic brain injury. 
  • The role of interferon-β in the treatment of multiple sclerosis and experimental autoimmune encephalomyelitis - in the perspective of inflammasomes. 
  • Thioredoxin-interacting protein mediates ER stress-induced β cell death through initiation of the inflammasome. 
  • Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. 
  • YopM puts caspase-1 on ice. 
  • [NLRP3 inflammasome and multiple sclerosis/EAE]. 
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  Keywords of People

  • Miao, Edward A., Professor of Integrative Immunobiology, Cell Biology
  • Shinohara, Mari L., Professor of Integrative Immunobiology, Cell Biology