Deregulated inflammasome signaling in disease
- Biology, MedicineImmunological reviews
The role of inflammasomes in regulating innate and adaptive immune responses is reviewed with an emphasis on the role of these immune complexes in autoinflammatory disorders and autoimmune diseases such as colitis, type I diabetes, multiple sclerosis and vitiligo.
The inflammasome NLRs in immunity, inflammation, and associated diseases.
- Biology, MedicineAnnual review of immunology
Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge, and a review presents and integrates recent progress in the field.
Molecular Mechanism of NLRP3 Inflammasome Activation
- BiologyJournal of Clinical Immunology
Three signaling pathways involving potassium efflux, generation of reactive oxygen species, and cathepsin B release are discussed, which drive innate immune response towards invading pathogens and cellular damage, and regulates adaptive immune response.
Molecular mechanisms regulating NLRP3 inflammasome activation
- Biology, MedicineCellular and Molecular Immunology
The NLRP3 inflammasome is linked with various human autoinflammatory and autoimmune diseases and may be a promising target for anti-inflammatory therapies, according to current understanding of the mechanisms by which it is activated in the cytosol.
Emerging inflammasome effector mechanisms
- BiologyNature Reviews Immunology
These non-canonical functions of caspase 1 illustrate the diverse mechanisms by which inflammasomes might contribute to innate immunity, repair responses and host defence.
Inflammasomes and Colorectal Cancer
This work reviews extant studies delving into different functions of inflammasomes in colorectal cancer development and concludes that infammasomes play contradictory roles in the development of inflammation-induced cancers.
Inflammasomes as Targets for Adjuvants
- Biology, MedicinePathogens
This review is focused on the mechanisms of action and the effects of adjuvants on inflammasome activation, which are necessary for the development of a healthy immune response against infectious diseases.
Post-translational regulation of inflammasomes
- Biology, MedicineCellular & Molecular Immunology
This review focuses on the emerging roles of post-translational modifications (PTMs) that regulate activation of the NLRP3, NLRP1, NLRC4, AIM2 and IFI16 inflammasomes.
Evasion of inflammasome activation by microbial pathogens.
- Biology, MedicineThe Journal of clinical investigation
This Review discusses a number of pathogens that have developed strategies to evade inflammasome activation as well as the potential infectious complications of therapeutic blockade of IL-1 pathways.
The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases
- BiologyFrontiers in Aging Neuroscience
The recent advances in understanding theNLRP3 mechanism, its role in disease pathology, and a broad review of therapeutics discovered to target the NLRP3 pathway and their challenges are discussed.
SHOWING 1-10 OF 131 REFERENCES
The inflammasomes: guardians of the body.
- BiologyAnnual review of immunology
The role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease are discussed.
Thioredoxin-interacting protein links oxidative stress to inflammasome activation
- Biology, MedicineNature Immunology
The participation of TXNIP in the NLRP3 inflammasome activation may provide a mechanistic link to the observed involvement of IL-1β in the pathogenesis of type 2 diabetes.
The NLRP3 Inflammasome: A Sensor for Metabolic Danger?
- Biology, MedicineScience
It is proposed that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.
T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes
- Biology, MedicineNature
An unexpected mechanism of inflammasome inhibition is revealed, whereby effector and memory T cells suppress potentially damaging inflammation, yet leave the primary inflammatory response, crucial for the onset of immunity, intact.
Cryopyrin activates the inflammasome in response to toxins and ATP
It is shown that cryopyrin-deficient macrophages cannot activate caspase-1 in response to Toll-like receptor agonists plus ATP, the latter activating the P2X7 receptor to decrease intracellular K+ levels.
Inflammatory caspases and inflammasomes: master switches of inflammation
- BiologyCell Death and Differentiation
The role of inflammasomes and inflammatory caspases in innate immunity against pathogens, autoinflammatory syndromes and in the biology of reproduction is highlighted, underlining the importance of the NLR family members, NALPs, NAIP and IPAF.
Critical function for Naip5 in inflammasome activation by a conserved carboxy-terminal domain of flagellin
- BiologyNature Immunology
It is demonstrated that 35 amino acids of the carboxyl terminus of flagellin triggered inflammasome activation in the absence of bacterial contaminants or secretion systems, clarifying the molecular basis for the cytosolic response to flageLLin.
Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression1
- BiologyThe Journal of Immunology
It is shown that cell priming through multiple signaling receptors induces NLRP3 expression, which is identified to be a critical checkpoint for NLRP2 activation and signals provided by NF-κB activators are necessary but not sufficient forNLRP3 activation.
The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.
- BiologyMolecular cell
Activation of the IL-1beta-processing inflammasome is involved in contact hypersensitivity.
- BiologyThe Journal of investigative dermatology
It is shown that key components of the inflammasome are present in human keratinocytes and that CS like trinitro-chlorobenzene induce caspase-1/ASC dependent IL-1beta and IL-18 processing and secretion, and that ASC- and NALP3-deficient mice display an impaired response to CS.