nflammasomes are scaffolds that are assembled in the host cytosol to cope with pathogens and cellular stress. The pattern-recognition receptors NLRP1, NLRP3, NLRC4, AIM2 and Pyrin all assemble distinct inflammasome platforms that contribute to host defense through proteolytic maturation and secretion of the inflammatory cytokines interleukin-(IL)1β and IL18, and by inducing pyroptosis, a pro-inflammatory regulated cell death mode. Unlike in infections, however, inflammasome activation is detrimental in the context of many chronic autoinflammatory diseases. Here, we investigated inflammasome regulatory mechanisms in the context of autoinflammation in murine models and patients.
Mo Lamkanfi obtained his PhD in Biotechnology at Ghent University in 2004, and enjoyed postdoctoral training in immunology with Dr. Gabriel Nunez at the University of Michigan, as well as with Dr. Vishva Dixit at Genentech in San Francisco. He returned to Belgium in 2009, where he currently heads the ‘NOD-like receptor and inflammasome laboratory’ of VIB (the Flanders Institute of Biotechnology). He also is affiliated with the Department of Internal Medicine of Ghent University.
His research group studies the roles of ‘NOD-like receptors’ and ‘inflammasomes’ in infections, inflammatory and autoimmune diseases, and has described various mechanistic aspects of NLR and inflammasome signaling. He contributed to over 100 studies in the inflammasome field, and his recent recognitions and awards are an ‘ERC Starting grant’ (2011) and an ‘ERC Consolidator Grant’ (2015); the Prize of the Flemish Scientific Foundation for Biomedical Sciences (2013); the AstraZeneca Foundation Prize for Auto-immune diseases and Rheumatology (2014); and the Baillet Latour Grant for Medical Research (2016).