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0000-0002-5704-582X
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- Rudi Beyaert is full professor at the Ghent University and Deputy Science Director at the VIB Center for Inflammation Research (Belgium) where he also leads the Unit of Molecular Signal Transduction in Inflammation Research. R. Beyaert has a track record of >30 years in molecular and cellular mechanism of inflammation and immunity. His most important discoveries include the role of MyD88 alternative splicing in TLR signalling, the anti-inflammatory role and mechanism of action of A20 (TNFAIP3), the discovery and characterization of ABIN (TNIP)-1, -2, -3 as ubiquitin-binding proteins and key regulators of inflammation, the development of IL-33 and TSLP cytokine traps, and the discovery of MALT1 paracaspase activity, which have inspired research in many labs worldwide. The Beyaert lab’s discovery that MALT1 plays a key role in innate and adaptive immune signalling has also triggered the development of MALT1 inhibitors for the treatment of cancer and autoimmune disease by several big pharma companies. Ongoing research mainly focuses on the molecular mechanisms that regulate immunity at epithelial barrier surfaces of the lung, skin and gut, and which are involved in inflammatory disease (asthma, psoriasis, inflammatory bowel disease) and immunodeficiency. We are also interested in genetic and environmental factors that contribute to IBD development in humans. In our research we are following an integrated molecular and immunological approach, combining functional studies on in vitro/ex vivo mouse and human cellular models with detailed phenotyping of gene targeted mice. R. Beyaert authors over 300 peer-reviewed papers that have been cited >30 000 times (h-index 89), and 19 book chapters. He is also inventor on >15 patent applications, and expertise and research of the Beyaert lab contributed to 2 VIB spin-offs (Aelin Therapeutics, 2017; Dualyx, 2020). His work has been recognized by a number of awards, including the Pfizer award and the five-yearly Prize of Fundamental Medical Sciences of the Belgian Royal Academy of Medicine. R. Beyaert was also recognized by Clarivate as ‘Highly Cited Researcher’ in the field of Immunology in 2022 and 2023. R. Beyaert is teaching several courses in the Bachelor and Master programme in Biochemistry and Biotechnology of the Ghent University. R. Beyaert has also shown strong leadership in the training and advancement of young scientists: 39 PhD students and 23 postdocs were trained in his lab, most of which have afterwards taken up important positions in academia (39%), industry (32%) or consulting (16%). Six of his former trainees now hold professor or assistant professor positions. R. Beyaert is on the editorial board of ‘The FEBS Journal’ and ‘Biochem. Pharmacol.’, and serves as an expert panel member for multiple national/international science funding organizations (including Advanced ERC). R. Beyaert has been involved in several national and international research consortia or infrastructures. Since 2006 he is also coordinating the BCCM GeneCorner plasmid collection, which is Europe’s most active public resource of plasmids and host strains serving labs worldwide. Five most important achievements in the last 10 years: 1. We demonstrated a role of MALT1 in preclinical models of MS (McGuire et al., J. Immunol., 2013; McGuire et al., J. Neuroinfl., 2014), arthritis (Gilis et al., Arthr. Rheum., 2019 +journal cover), psoriasis (Van Nuffel et al., EMBO Rep, 2020), viral neuroinflammation (Kip et. J Virol, 2018a and 2018b). 2. We made the surprising finding that germline inactivation of MALT1 proteolytic activity results in destructive autoimmunity, which was however not observed when MALT1 was inhibited post-birth (Demeyer et al., Front Immunol, 2019; Demeyer et al., iScience, 2020). 3. We discovered 2 novel MALT1 substrates (Staal et al., EMBO J., 2011; Elton et al., FEBS J, 2016; Skordos et al., FEBS J, 2023) and showed a functional interaction of MALT1 with CARD14 in vitro (Afonina et al., EMBO Rep, 2016) and in vivo (Van Nuffel et al., EMBO Rep, 2020). 4. We engineered novel cytokine antagonists (IL33trap; Holgado et al., JACI, 2019 + patent); TSLPtrap (Verstraete et al., Nature Comm, 2017 + patent); IL4/13trap (Holgado et al., Front Immunol, 2020) that may complement therapeutic monoclonal antibodies. 5. We described the important role of A20 in tissue homeostasis and disease in preclinical models (Matmati et al., Nature Gen., 2011; Maelfait et al., Plos Pathog., 2012; Vereecke et al., Nature Comm., 2014; Vande Walle et al., Nature, 2014; Schuijs et al., Science, 2015; Martens et al., Nature Immunol., 2020; Holgado et al., J Allergy Clin Immunol, 2023).
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The phytohormone abscisic acid enhances remyelination in mouse models of multiple sclerosis
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NF-κB regulated expression of A20 controls IKK dependent repression of RIPK1 induced cell death in activated T cells
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Interleukin-33-activated basophils promote asthma by regulating Th2 cell entry into lung tissue
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CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation
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Polo-like kinase 1 (PLK1) is a novel CARD14-binding protein in keratinocytes
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Chimeric and mutant CARD9 constructs enable analyses of conserved and diverged autoinhibition mechanisms in the CARD-CC protein family
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Laboratory mice with a wild microbiota generate strong allergic immune responses
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The impact of hepatocyte-specific deletion of hypoxia-inducible factors on the development of polymicrobial sepsis with focus on GR and PPARα function
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Exploring species-specificity in TLR4/MD-2 inhibition with amphiphilic lipid a mimicking glycolipids
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Proteolytic activity of the paracaspase MALT1 is involved in epithelial restitution and mucosal healing