Proteases from diverse viruses, the first described pathogen-encoded activators of human NLRP1, cleave NLRP1 at a sequence that mimics the viral polyprotein, resulting in inflammasome activation and pro-inflammatory cytokine release.
Characterization of the effects of complement- and inflammasome-mediated inflammation on choroidal neovascularization in a mouse model of neovascular age-related macular degeneration suggests synergistic benefits from targeting both forms of inflammation.
A new mode of inflammasome regulation was discovered through a mouse strain intercross that identified the Pycard locus was associated with IL-1β release, and gene editing showed this was due to an SNP in the Pycard mRNA regulating its turnover.
Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.
A novel pathway was discovered for cellular uptake of LPS through secretory protein secretoglobin3A2 and a receptor syndecan-1, causing activation of non-canonical inflammasome pathway leading to pyroptosis of cancer cells.
Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na+) channels.