«Innate sensing of danger by inflammasomes»

12.03.2026 12:30 – 13:30

Innate immunity translates danger signals into inflammatory responses that protect the host. However, when dysregulated, overactive or chronic innate immune activation becomes a key driver of many common inflammatory diseases. This lecture focuses on inflammasomes, key cytosolic sensing platforms that activate caspase-1, promote IL-1β and IL-18 maturation, and induce pyroptotic cell death. Inflammasomes are at the center of a mechanistic framework for sterile inflammation and a better molecular understanding of their activation mechanism will enable insights into disease processes.

The lecture describes how diverse disease-relevant perturbations converge on inflammasome assembly, with emphasis on NLRP3 and NLRP1 as integrators of sterile inflammatory cues. It discusses upstream stress pathways and cellular “danger hubs,” including ionic flux, mitochondrial dysfunction, lysosomal damage, metabolic imbalance, redox stress, and activation by particulate or crystalline stimuli. Using examples across cardiometabolic inflammation, rheumatic and neuroinflammatory diseases, autoinflammatory syndromes, and infection-associated immunopathology, the lecture highlights how tissue context, priming signals, and regulatory checkpoints determine the magnitude, timing, and consequences of inflammasome activation and how these factors define actionable molecular endotypes.

Finally, the talk outlines translational opportunities enabled by these insights, including direct inflammasome inhibitors, modulation of upstream licensing pathways, and IL-1/IL-18–targeted strategies. It also addresses how biomarker-guided stratification and mechanism-based patient selection can increase precision, maximize efficacy, and reduce unwanted immune suppression in next-generation anti-inflammatory therapies.

Lieu

Bâtiment: CMU

Auditoire Müller

entrée libre

Fichiers joints

afficheA3_FIB_Latz_2.pdf

177.2 Kb