Inflammasomes

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  Subject Areas on Research

  • A CRISPR-Cas system enhances envelope integrity mediating antibiotic resistance and inflammasome evasion. 
  • A noncanonical function of cGAMP in inflammasome priming and activation. 
  • 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. 
  • 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. 
  • Canonical Inflammasomes Drive IFN-γ to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium. 
  • Control of the innate immune response by the mevalonate pathway. 
  • Elevated hydrostatic pressure stimulates ATP release which mediates activation of the NLRP3 inflammasome via P2X4 in rat urothelial cells. 
  • Frontline Science: Multiple cathepsins promote inflammasome-independent, particle-induced cell death during NLRP3-dependent IL-1β activation. 
  • 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. 
  • IKKα negatively regulates ASC-dependent inflammasome activation. 
  • Immune activation by histones: plusses and minuses in inflammation. 
  • 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, Inflammation, and Tissue Homeostasis. 
  • Inflammasomes are important mediators of cyclophosphamide-induced bladder inflammation. 
  • Inflammasomes in the urinary tract: a disease-based review. 
  • Innate Immune Cell Recovery Is Positively Regulated by NLRP12 during Emergency Hematopoiesis. 
  • Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome. 
  • Megalin/Cubulin-Lysosome-mediated Albumin Reabsorption Is Involved in the Tubular Cell Activation of NLRP3 Inflammasome and Tubulointerstitial Inflammation. 
  • Metabolic dysfunction in lymphocytes promotes postoperative morbidity. 
  • Mitochondrial Quality Control as a Therapeutic Target. 
  • Necroptosis-independent signaling by the RIP kinases in inflammation. 
  • Necrosis-dependent and independent signaling of the RIP kinases in inflammation. 
  • Participation of c-FLIP in NLRP3 and AIM2 inflammasome activation. 
  • Programmed necrosis in the cross talk of cell death and inflammation. 
  • Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis. 
  • 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 Role of Cell Death in the Pathogenesis of SLE: Is Pyroptosis the Missing Link? 
  • The Yersinia pestis Effector YopM Inhibits Pyrin Inflammasome Activation. 
  • The role of interferon-β in the treatment of multiple sclerosis and experimental autoimmune encephalomyelitis - in the perspective of inflammasomes. 
  • Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. 
  • [NLRP3 inflammasome and multiple sclerosis/EAE]. 
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  Keywords of People

  • Shinohara, Mari L., Associate Professor of Immunology, Immunology