The non-canonical inflammasome, comprising caspase-4 in humans, initiates pyroptosis upon sensing cytosolic lipopolysaccharide (LPS) from Gram-negativ…

Cette année, trois jeunes scientifiques viennent renforcer la Faculté de biologie et de médecine (FBM) de l’Unil. Lauréat·es des subsides Ambizione du Fonds national suisse, Ella Hartenian, David Robe...

The EMBO Journal - The ability of intracellular bacteria to spread directly from one cell to the next, avoiding extracellular immune defenses and drugs, is essential for pathogen dissemination and,...

imageimageNINJ1 blocks HSV-1 entry into mouse macrophages independent of its role in cell death, resulting in greater secretion of pro inflammatory cytokines downstream of infection. Mouse macrophages lacking NINJ1 are more permissive to HSV-1 ...

en génomique des maladies infectieuses intracellulaires Chaire dexcellence / Full Professor or Associate Professor in Genomics of Intracellular Infectious Diseases Chair of Excellence

imageimageAvailable caspase-4/11 (CASP4/11) inhibitors also block the activity of caspase-1 (CASP1), which complicates interpretation of results in functional studies and limits their clinical potenti...

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NLRP6 controls host defense against bacteria and viruses in the gastrointestinal tract by a poorly understood mechanism. Here, we report that NLRP6 forms an inflammasome upon endolysosomal damage caus...

A loss-of-function genetic screen identifies the ER-resident protein CCDC134 as an essential regulator of Toll-like receptor (TLR) responses. CCDC134 binds

Nature Immunology - Pyroptotic cell death results in inflammation. Here the authors find that F-actin-rich structures formed during macrophage pyroptosis persist after cell death to activate...

H. polygyrus glutamate dehydrogenase drives parasite chronicity by epigenetically and metabolically reprogramming host macrophages.

Pyroptotic cell death results in inflammation. Here the authors find that F-actin-rich structures formed during macrophage pyroptosis persist after cell death to activate dendritic cells.