Our research is situated at the borderline between molecular biology and medicine. We are interested in the molecular mechanisms that control initiation, progression and resolution of inflammation and immunity. Further insight into these molecular mechanisms raises the prospect for better understanding and rational design of therapeutics for several diseases, including autoimmunity, allergy and cancer. In our research we make use a variety of biochemical, molecular and cellular approaches combined with mouse gene targeting and mouse models of human disease (e.g. multiple sclerosis, rheumatoid arthritis, Crohn’s disease, psoriasis, sepsis).
More specifically we are studying major intracellular signaling pathways (such as NF-κB signaling) that control gene expression in response to specific cytokine receptors (TNF, IL-1, IL-33), pattern recognition receptors (TLR4), and T cell antigen receptors. We have a particular interest in the role of protein-protein interactions and posttranslational modifications such as protein ubiquitination and phosphorylation. Our lab has made a significant contribution to the understanding of the mechanism of action and the physiological significance of the NF-kB inhibitory protein A20 (=TNFAIP3) in multiple cell types and diseases including rheumatoid arthritis and colitis. In addition, we discovered that the paracaspase MALT1, which is pivotal in antigen receptor-mediated lymphocyte activation and lymphomagenesis, has a unique proteolytic activity. This finding is now being validated and translated into therapeutics for human disease in collaboration with the pharmaceutical industry.
In collaboration with experts within and outside of IRC we are pursuing to study the molecular mechanisms that mediate and regulate the activity of A20, MALT1 and several other newly identified signaling proteins in the context of innate and adaptive immunity. We also exploit our knowledge and expertise in signaling to identify key molecules affecting phagosome function and the intracellular fate of antigens. Finally, based on innovative protein engineering approaches our research group is also developing novel biological tools that allow to interfere with the function of different cytokines and to treat immune-system related disease.
PhD students Anne-Marie Pauwels, Aurora Holgado from the Rudi Beyaert lab participate in the European project "Tollerant" that was presented on the EXPO2015 in Milan. It resulted in "The wonderful journey of a molecule in our body: from drugs to functional food". Their contribution starts at 5':05".
25/04/2016 - Psoriasis is a long-lasting autoimmune disease that is characterized by patches of abnormal and inflamed skin. It is generally thought to have a genetic origin, which can be further triggered by environmental factors.
18/12/2015 - Phagocytosis represents a critical innate barrier against infection and serves the clearance of extracellular microbes, infected and dying cells. The results are published in the December issue of the prestigious journal Immunity.
31/01/2014 - VIB and CD3 (KU Leuven) today announced the signing of a license and collaboration agreement with AstraZeneca for the development of novel MALT1 inhibitors as therapeutics in inflammatory and oncological diseases.
09/10/2012 - Scientists (VIB/UGent) have discovered a mechanism used by the protein A20 to combat inflammation. This could be a very important point of focus in the search for a treatment for autoimmune diseases such as Rheumatoid Arthritis.
16/08/2011 - In Nature Genetics, VIB-UGent researchers demonstrate that a defect in the expression of the A20 gene can contribute to the development of rheumatoid arthritis in mice, identifying A20 as a target for the generation of new drugs.
05/07/2010 - Scientists associated with VIB and Ghent University (UGent) have discovered that A20 protein plays an important protective role in diseases associated with chronic bowel inflammation.
28/01/2008 - VIB researchers have elucidated the function of MALT1, a key player in controlling inflammatory reactions. They are the first to show that MALT1 is able to cleave the A20 protein, which inhibits inflammation.