Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*).

By S. Masters, A. Simon, I. Aksentijevich, Daniel L. Kastner. Annual Review of Immunology, 2009

1,096 citations recorded by the source corpus.

Subfields: Hematology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7154bfca2d484ba9b494f95bca468ca552251dba

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Citations in the corpus

NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, background): “…Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France b CNRS-UMR 8256, F-75005 Paris, France c Inserm U1164, F-75005 Paris, France d Institute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, D-89081 Ulm, Germany a r t i c l e i n f o”
Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome. (2016, background): “Asterisk, mouse Ser 291. unoprecipitated with anti-Flag for PKA-induced phosphorylation and ubiquiti- tion of HA-ASC, Myc-pro-caspase-1, pro-IL-1b, and Flag-NLRP3, Flag-NLRP3 LRP3 wild-type, NLRP3 S291A, NLRP3 S219D, or NLRP3 S291E as indicated. rent CAPS-associated Flag-tagged NLRP3 mutants as indi”
Human Monocytes Engage an Alternative Inflammasome Pathway. (2016, neutral): “…involvement in pathogen clearance and immune homeostasis, aberrant IL-1b production is associated with monogenetic auto-inflammatory diseases (Masters et al., 2009), but also with ligand-dependent, multifactorial, sterile inflammatory conditions, such as atherosclerosis, type 2 diabetes,…”
The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “In fact, over 90 diseaseassociated mutations have since been observed in humans in and around the NBDs that render NLRP3 constitutively active (Masters et al., 2009).”
The sterile inflammatory response (2010, background): “Many mutations within NALP3 have been described in patients with the auto-inflammatory diseases Muckle-Wells syndrome (MWS), familial cold autoinflammatory syndrome (FCAS) and chronic neurologic cutaneous and articular syndrome (CINCA) (80).”
Anti-inflammatory Agents: Present and Future (2010, positive): “Mutations associated with the classic autoinflammatory disease familial Mediterranean fever also increase the secretion of IL-1b (Masters et al., 2009).”
Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression1 (2009, background): “Notably, 40% of patients with autoinflammatory diseases present with classical clinical symptoms without carrying any mutations in the coding region of NLRP3 (17).”
Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. (2011, background): “(6) Caspase-1 is activated by the inflammasome, cleaves the IL-1 precursor, and mature, active IL-1 is released.”
Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome (2010, background): “NLRP3, also known as cryopyrin, forms an inflammasome with the adaptor molecule ASC and caspase-1 to convert pro-IL-1β and pro-IL-18 into their active forms. Mutations in NLRP3 lead to chronic autoinflammatory syndromes.”
The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “Single mutations are associated with multiple clinical syndromes, suggesting either additional modifying loci or environmental factors (20).”