Lieselotte Vande Walle

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: The precise mode of action and importance of cytochrome c in apoptosis in mammalian cells has become clear through biochemical, structural and genetic studies, and more recently identified factors, for example HtrA2/OMI and Smac/DIABLO, are still being studied intensively in order to delineate their functions in apoptoses.

TL;DR: Loss of FADD or caspase-8 in a RIP3-deficient background, but not RIP3 deficiency alone, hampered transcriptional priming and posttranslational activation of the canonical and noncanonical Nlrp3 inflammasome.

TL;DR: It is shown that mice lacking both IL-1β and IL-18 are normally susceptible to LPS-induced splenocyte apoptosis and endotoxic shock, and the existence of another caspase 1-dependent mediator of endotoxemia is indicated.

TL;DR: A20 is revealed as a novel negative regulator of Nlrp3 inflammasome activation, and A20myel-KO mice is described as the first experimental model to study the role of inflammaomes in the pathology of rheumatoid arthritis.