Eva Bartok

TL;DR: It is found that NLRP3 inflammasome activation strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors, and these data do not exclude a general role for ROS production in the process ofNLRP3-triggered inflammation, but they would put ROS upstream of NL RP3 induction, but not activation.

TL;DR: Current knowledge of mechanisms leading to the activation of inflammasomes is reviewed and the controversial molecular mechanisms that regulate NLRP3 signaling are focused on and recent advancements in DNA sensing by the inflammaome receptor AIM2 are highlighted.

TL;DR: The number of infections in this high prevalence community is not representative for other parts of the world, but the IFR calculated on the basis of the infection rate in this community can be utilized to estimate the percentage of infected based on the number of reported fatalities in other places with similar population characteristics.

TL;DR: It is shown that the human monocytic cell line THP1 activates the inflammasome in response to cytosolic LPS in a TLR4‐independent fashion, providing evidence for the presence of a non‐canonical inflammaome in humans and its dependence on caspase‐4.

TL;DR: It is shown that the methylation status of endogenous capped mRNA at the 5′-terminal nucleotide (N1) was crucial to prevent RIG-I activation and a new role for cap N1-2′O-methylation in Rig-I tolerance of self-RNA is revealed.