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 promotes expansion of SLC2A1highSPP1highIFNlow myeloid cells that drive immune escape and malignant transformation in precancerous head and neck lesions.
AMBRA1 allosterically activates NLRP3 by destabilizing its autoinhibited conformation, promoting transition to an active state in inflammatory responses.
Covalent caspase inhibitors delivered via GSDMD pores effectively suppress pyroptosis and cytokine release, offering a targeted approach for inflammatory disease treatment.
NLRP3 inflammasome interacts with multiple innate immune pathways and cell death mechanisms, shaping inflammatory responses during pathogen infection.
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ExoU secreted by P. aeruginosa increases lysophosphatidylcholine levels, activating inflammasomes and causing cell death, with significant implications for cystic fibrosis infections.
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Aurora A kinase enhances inflammasome activation, increasing inflammation and bacterial survival in antibiotic-resistant Staphylococcus aureus infections.
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Proteolytic activation of caspase-3 and caspase-7 is essential for distinct physiological processes in mice, with activation controlling different functions in adult tissues.
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Topics moving, week to 23 Oct 2026
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