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The ability to sense and respond to danger appropriately is critical for maintaining immune homeostasis. Inflammasomes are supra-molecular protein complexes that sense danger signals both from microbes and tissue damage, and initiate an inflammatory response through activation of the protease caspase-1 and subsequent release of interleukin(IL)-1β and IL-18. Dysregulation of inflammasomes contributes to the progression of chronic disease such as Alzheimer’s disease, COPD, or Rheumatoid Arthritis.
In this seminar we will discuss our latest work on the molecular mechanisms that control inflammasome activation in macrophages, especially the contribution of posttranslational modifications to this process.
