Mo Lamkanfi was born in Antwerp in 1978, and received a degree in biochemistry from Ghent University in 2000. He obtained his PhD in biotechnology from the same university in 2004, and subsequently moved to the USA, where he enjoyed postdoctoral training in immunology at the University of Michigan (Ann Arbor, MI) and at the biotechnology company Genentech (San Francisco, CA).
Prof. Lamkanfi returned to Ghent in 2009, where he is now affiliated with the Department of Internal Medicine of Ghent University. He is also Group leader at VIB (the Flanders Institute of Biotechnology), where he heads the ‘NOD-like receptor and inflammasome laboratory’ at the Inflammation Research Center (IRC). Prof. Lamkanfi authored over 95 scientific publications on inflammasome research, and 3 patent applications. His recent recognitions and awards are a ‘Starting grant’ (2011) and an ‘ERC Consolidator Grant’ (2015) of the European Research Council (ERC); the Prize of the Flemish Scientific Foundation for Biomedical Sciences (2013); and the AstraZeneca Foundation Prize for Auto-immune diseases and Rheumatology (2014).
PyroPop - Mechanisms and regulation of inflammasome-associated programmed cell death
Regulated cell death is an important mechanism that enables immune cells to resist microbial pathogens. In the context of an infection, immune cells can die by means of pyroptosis - a lytic form of cell death that is dependent on inflammasomes – to expose the pathogen to other immune cells. This form of cell death also is associated with the secretion of cytokines that trigger inflammation, and release of other factors that alert immune cells of imminent danger. In contrast, apoptosis constitutes a cell death mechanism by which a strong immune stimulation is avoided because the cell content is taken up and recycled by other cells during the cell death process. The central objective of ERC project PyroPop is to determine how inflammasomes link the detection of pathogens to regulated cell death with different immunologic outcomes. Elucidation of mechanisms by which inflammasomes induce pyroptosis and apoptosis holds promise for the development of an entirely novel therapeutic concept. My group wants to use the newly to be acquired knowledge to convert pyroptosis, which provokes inflammation, into apoptosis, which does not cause inflammation, in autoimmune and autoinflammatory diseases where inflammatory responses are destructive.
