Inflammasome and immune disorders

This study identifies UBXN1's role in activating the non-canonical inflammasome via unanchored ubiquitin chains, showing its importance in sepsis and inflammasome signaling.

This study examines the evolutionary history of pro-inflammatory caspases in primates and rodents, revealing differences in gene retention, pseudogenization, and positive selection across species.

The paper identifies a Pseudomonas aeruginosa VgrG2b fragment cleaved by caspase-11 that inhibits NLRP3 inflammasome activation, promoting infection and improving survival with a specific peptide inhibitor.

The paper identifies retention of 129S genome in Nlrp3-/- mice causing NLRP1 hypersensitivity and transcriptional changes, and introduces a conditional Nlrp3 allele to resolve phenotypes.

The paper identifies a new ALPK1 variant causing ROSAH syndrome and shows it has altered activation by different metabolites, explaining autoinflammatory episodes.

This study examines age-associated inflammasome activation in multiple tissues, finding tissue-specific differences in transcriptional and post-translational inflammatory responses.

The paper shows that butyrate and propionate activate the NLRP3 inflammasome in human macrophages when combined with TLR agonists, through HDAC inhibition and epigenetic changes.

This study shows methylglyoxal, a glycolytic metabolite, covalently inactivates the NLRP3 inflammasome by forming crosslinks, thereby reducing inflammation.

This study shows that alveolar macrophages worsen influenza-induced lung injury in a human lung alveolus chip, but blocking pyroptosis reduces inflammation and tissue damage.

This study shows that NLRP1B allele 2 in intestinal epithelial cells does not respond to VbP, unlike in macrophages, suggesting allele-dependent regulation in IECs.

The paper identifies NLRP3, NLRP6, and NLRP12 as inflammasomes with distinct expression patterns and activation mechanisms in different cell types.

This study identifies EseB, a T3SS translocon protein, as a direct activator of the NLRC4/NAIP inflammasome, inducing pyroptosis in host cells through a conserved mechanism across T3SS-positive bacteria.

The paper identifies that NLRP3 binds and cleaves oxidized DNA, and small molecule drugs inhibit this process to prevent inflammasome activation.

The paper investigates four CDC42 variants in autoinflammatory patients, showing that C-terminal variants cause actin defects and NF-kB hyperactivation, while the N-terminal variant does not.

This study shows high concentrations of atazanavir induce mitochondrial dysfunction and NLRP3 inflammasome/pyroptosis in T cells, leading to apoptosis.

This study shows HCoV-229E Mpro inactivates GSDMD to block pyroptosis but promotes lytic cell death, partially via GSDME and caspases-3/-8.

This study shows perforin triggers pyroptosis in target cells by activating the NLRP3/caspase-1/gasdermin D pathway, while sustained CTL interaction leads to apoptosis.

This study shows the NLRP3 inflammasome is crucial for IL-18 production in a murine model of MAS but not for other disease features.

This study profiles proteomic changes in subcellular compartments during NLRP3 inflammasome activation and identifies disruptions in retrograde trafficking pathways.

The paper identifies that pathogenic NLR mutations cause PELO-independent ATPase activation, leading to inflammatory responses and disease, and suggests this as a diagnostic marker.

This study shows human NK cells can activate inflammasomes in vitro and in transplant patients, with distinct responses in CD56 subsets and sustained activation in renal dysfunction and transplant rejection.

This study identifies biallelic RIPK1 activating variants causing autoinflammatory disease through T cell death and cytokine amplification.

The paper shows that cytosolic sodium accumulation triggers NLRP3 inflammasome activation in response to various danger signals in human macrophages.

This study identifies brazilin as a natural product inhibitor of the NLRP3 inflammasome, effective in multiple models and suggesting its potential as a therapeutic scaffold.

This study shows that WTAP promotes LPS-induced pyroptosis and inflammation in endothelial cells by enhancing NF-κB p50 function and facilitating its interaction with NLRP3.

A genome-wide CRISPR screen and genetic analysis identify TNRC18 as a novel regulator of IL-1β production and a risk factor for inflammatory diseases.

This paper shows etifoxine inhibits NLRP3 inflammasome activity in human and murine myeloid cells, with anti-inflammatory effects independent of its known TSPO and GABAA receptor interactions.

The paper identifies two distinct NLRP3 activation pathways, one dependent on decameric cage formation and another independent of the MTOC and TGN.

This study identifies how different GSDMB isoforms and protease cleavage regulate pyroptosis and mitochondrial damage in cancer cells.

This study identifies DPP9 deficiency as a Mendelian disorder causing inflammasome hyperactivity, which can be rescued by reducing NLRP1/IL-1 signaling in mice.