Wyne P. Lee

TL;DR: It is shown that cryopyrin-deficient macrophages cannot activate caspase-1 in response to Toll-like receptor agonists plus ATP, the latter activating the P2X7 receptor to decrease intracellular K+ levels.

TL;DR: It is shown that gasdermin D is essential for caspase-11-dependent pyroptosis and interleukin-1β maturation and a key mediator of the host response against Gram-negative bacteria.

TL;DR: It is shown, with C57BL/6 Casp11 gene-targeted mice, that caspase-11 is critical for casp enzyme-1 activation and IL-1β production in macrophages infected with Escherichia coli, Citrobacter rodentium or Vibrio cholerae, and a unique pro-inflammatory role for casingase- 11 in the innate immune response to clinically significant bacterial infections is highlighted.

TL;DR: Interestingly, cell death triggered by stimuli that engage caspase-1 was ablated in macrophages lacking either ASC or Ipaf, suggesting a coupling between the inflammatory and cell death pathways.

TL;DR: It is shown that macrophages loaded with synthetic lipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like receptor 4 (TLR4), revealing a TLR4-independent mechanism for innate immune recognition of LPS.