Related Experiment Video
Updated: Apr 12, 2026

06:52
Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
11.4K
The Nlrp3 inflammasome admits defeat
1Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.
Trends in Immunology
|May 21, 2015
Summary
The Nlrp3 inflammasome, crucial for immune responses, can be specifically inhibited by MCC950 and β-hydroxybutyrate. These findings offer new therapeutic avenues for treating autoinflammatory diseases.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- The Nlrp3 inflammasome is a key mediator of inflammatory responses, triggering interleukin-1 (IL-1) secretion from myeloid cells.
- It is activated by a wide range of endogenous and exogenous danger signals, contributing to various inflammatory conditions.
Purpose of the Study:
- To highlight recent findings identifying specific inhibitors of the Nlrp3 inflammasome.
- To discuss the therapeutic potential of these inhibitors in autoinflammatory diseases.
Main Methods:
- Review of recent scientific literature identifying MCC950 and β-hydroxybutyrate.
- Analysis of their mechanisms as specific inhibitors of the Nlrp3 inflammasome.
Main Results:
- MCC950, a sulfonylurea compound, was identified as a specific Nlrp3 inflammasome inhibitor.
- β-hydroxybutyrate, a ketone metabolite, was also identified as a specific Nlrp3 inflammasome inhibitor.
Conclusions:
- Both MCC950 and β-hydroxybutyrate demonstrate promising therapeutic potential for autoinflammatory diseases.
- Targeting the Nlrp3 inflammasome represents a viable strategy for developing novel treatments for these conditions.
Related Concept Videos
Regulation of the Unfolded Protein Response
3.2K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K
The Unfolded Protein Response
7.1K
The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
7.1K
IP3/DAG Signaling Pathway
16.0K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
16.0K
NF-κB-dependent Signaling Pathway
10.7K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
10.7K
The Extrinsic Apoptotic Pathway
9.4K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.4K

