Type I interferons inhibit NLRP1-driven PANoptosis by reducing NLRP1 expression through a TLR4-TRIF-IRF3 signaling pathway.
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Inflammasome and immune disorders
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IL-1α drives expansion of SLC2A1highSPP1highIFNlow myeloid cells, promoting immune escape and malignant transformation in pre-cancerous head and neck lesions.
AMBRA1 allosterically activates NLRP3 by destabilizing its autoinhibited conformation, promoting inflammatory responses in mouse disease models.
NLRP3 inflammasome integrates innate immune signaling and cell death pathways, coordinating inflammatory responses and pyroptosis during infections and inflammation.
- Open access
ExoU secreted by P. aeruginosa increases lysophosphatidylcholine levels, activating inflammasomes and causing cell death, with significant implications for cystic fibrosis infections.
- Open access
Aurora A kinase enhances inflammasome activation, increasing inflammation and bacterial survival in antibiotic-resistant Staphylococcus aureus infections.
- Open access
Proteolytic activation of caspase-3 and caspase-7 is essential for distinct physiological processes in mice, with activation controlling different functions in adult tissues.
- Open access
CD8+ T cell immunity enhances tumor cell susceptibility to cuproptosis, improving the effectiveness of inducers in overcoming immunotherapy resistance in preclinical models.
- Open access
- 11 cites
Viral protease-initiated lytic cell death (VIDA) mRNA therapy effectively eliminates multiple viruses, including HAV, ZIKV, and SARS-CoV-2, by targeting infected cells.
Ahr1 transcription factor is essential for activating the NLRP3/IL-1β pathway, recruiting neutrophils, and clearing Candida albicans from the brain, with 100% dependence observed in vivo.
- Open access
Iron-dependent, protease-independent activation of gasdermin D drives IL-33 release and airway inflammation in allergic diseases, with a key role for ferritinophagy and iron chaperones.
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