Journal
CELL
Volume 157, Issue 5, Pages 1013-1022Publisher
CELL PRESS
DOI: 10.1016/j.cell.2014.04.007
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Funding
- Ghent University Concerted Research Actions [BOF14/GOA/013]
- European Research Council [281600]
- Fund for Scientific Research (FWO)-Flanders [G030212N]
- European Research Council (ERC) [281600] Funding Source: European Research Council (ERC)
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Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1 beta and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field.
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