Mice deficient in inflammasome adaptor molecule ASC are partially protected from acute weight loss after immunization with rVSV vaccine vectors Because the ultimate goal of these studies was to devise strategies by which we could suppress IL-1b production and thereby reduce the pathology of rVSV vectors in vivo, we sought to determine the mechanism by which IL-1b was being produced in response to VSV. IL-1b is synthesized as an inactive precursor molecule (pro-IL-1b), which must be cleaved either intracellularly by endogenous protease caspase-1 [25, 26, 27] , or extracellularly by matrix metalloprotease 9 [28] or other neutrophil [29] and mast cell-associated proteases [30] to become biologically active. It was shown recently that murine bone marrow derived dendritic cells (BMDC) infected with VSV in vitro produce IL-1b via formation of an inflammasome composed of RNA helicase RIG-I, adaptor molecule ASC, and caspase-1 [22] . Because the authors did not test whether RIG-I, ASC, and caspase-1 were required to produce IL-1b in response to VSV in vivo we used caspase-1-deficient and ASC-deficient mice to determine the effects of the absence of these molecules on acute pathology after rVSV immunization. It was not practical to test RIG-I deficient mice for IL-1b induction, because RIG-I deficient mice do not produce IFN in response to VSV and therefore rapidly succumb to infection [31] .