Inflammasome and immune disorders

This study shows that Yersinia-induced cell death and IL-1β release are driven by spatially and temporally distinct but functionally connected death complexes.

This study shows that fatty acid synthesis promotes NLRP3 inflammasome activation through palmitoylation of NLRP3, with no effect on AIM2 inflammasome activation.

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.

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

The paper identifies UCH-L1 as an NLRP3 interactor that modulates IL-1β production in human macrophages and microglia through proximity proteomics and functional assays.

This study shows SARS-CoV-2 viroporins ORF3a, E, and M activate inflammasomes in macrophages and induce IL-1α release in pulmonary epithelial and endothelial cells, contributing to immunothrombosis in COVID-19.

This study shows DENV NS1 activates inflammasomes in macrophages, leading to IL-1β release without pyroptosis, and that this pathway is protective against DENV infection.

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 identifies ZDHHC7-mediated palmitoylation of NLRP3 at Cys126 as critical for inflammasome activation, with implications for therapeutic targeting of inflammatory diseases.

This study shows that S-acylation of NLRP3's Cys-130 residue regulates its Golgi association through a nigericin-sensitive cycle, linking Golgi dysfunction to NLRP3 activation.

This study functionally characterizes 34 NLRP3 variants associated with CAPS, identifying functional diversity and inhibitor sensitivity, with implications for diagnosis and drug development.

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 identifies a transient disulfide bond between NLRP1 and oxidized TRX1, revealing how NLRP1 senses cellular redox state to regulate inflammasome formation.

This study shows doxorubicin causes bone loss via inflammasome activation, leading to pyroptosis and NETosis, and identifies AIM2 and NLRP3 as key mediators.

The paper shows that caspase-1 activates GSDMA in non-mammals like amphibians, reptiles, and birds, revealing an evolutionary shift in caspase-1's target gasdermin.

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.

This paper identifies proteolytic cleavage as the mechanism regulating fungal gasdermin activity, showing that HET-Q1 is cleaved by HET-Q2 to induce cell death and that gasdermin genes are clustered with protease genes.

This study shows that NLRP3 inhibition after reperfusion reduces brain injury in ischemia by protecting the blood-brain barrier and reducing inflammation.

The paper identifies a SNP in the 3' UTR of the Pycard gene in mice that affects mRNA stability and inflammasome activity through CRISPR/Cas9 editing.

The paper shows that PPARA upregulates Gm15441, which suppresses TXNIP and reduces NLRP3 inflammasome activation during metabolic stress.

This study identifies a novel mutation in A20 causing haploinsufficiency and shows it impairs the protein-protein interactome, leading to enhanced NLRP3 inflammasome activation through caspase-8.