Rudi Beyaert Lab

Research focus

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 plays a key role in innate and adaptive immunity as well as lymphoid malignancies, has a unique proteolytic activity that fine-tunes gene expression and cell activation.  Our preclinical studies have fostered the belief that MALT1 is a promising therapeutic target in autoimmunity and cancer. 

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.

Publications

Limiting inflammation-the negative regulation of NF-kappaB and the NLRP3 inflammasomeAfonina I* Zhong Z* Karin M* Beyaert R*NATURE IMMUNOLOGY, 18, 861-869, 2017* These authors contributed equally
The paracaspase MALT1 mediates CARD14-induced signaling in keratinocytesAfonina I, Van Nuffel E, Baudelet G, Driege Y, Kreike M, Staal J, Beyaert REMBO REPORTS, 17, 914-27, 2016
Toll-like Receptor 4 Engagement on Dendritic Cells Restrains Phago-Lysosome Fusion and Promotes Cross-Presentation of AntigensAlloatti A* Kotsias F* Pauwels A Carpier J Jouve M Timmerman E Pace L Vargas P Maurin M Gehrmann U Joannas L Vivar O Lennon-Duménil A Savina A Gevaert K Beyaert R* Hoffmann E* Amigorena S*IMMUNITY, 43, 1087-100, 2015* These authors contributed equally
A20 controls intestinal homeostasis through cell-specific activitiesVereecke L Araujo Vieira Da Silva S Billiet T Van Es J Mcguire C Slowicka K Sze M Van Den Born M De Hertogh G Clevers H Raes J Rutgeerts P Vermeire S Beyaert R* Van Loo G*Nature Communications, 5, 5103, 2014* These authors contributed equally
A20 inhibits LUBAC-mediated NF-kappaB activation by binding linear polyubiquitin chains via its zinc finger 7Verhelst K, Carpentier I, Kreike M, Meloni L, Verstrepen L, Kensche T, Dikic I, Beyaert REMBO JOURNAL, 31, 3845-55, 2012

Job openings

News

Research opens new treatment strategies for specific form of Psoriasis

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.

A novel mechanism that helps activated dendritic cells to initiate effective immunity

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.

VIB and CD3 enter into a License and Collaboration Agreement with AstraZeneca for the development of MALT1 inhibitors

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.

New point of focus found for the treatment of Rheumatoid Arthritis and other autoimmune 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.

Rudi Beyaert

Rudi Beyaert

Research area(s)

Model organism(s)

Bio

​PhD: Univ. of Ghent, Ghent, Belgium, 1992
VIB Group leader since 1997
Full Professor at Ghent University, Ghent, Belgium since 2003
Associate Department Director since 2009

Contact Info

VIB-UGent Center for Inflammation ResearchUGent-VIB Research Building FSVMTechnologiepark 927 9052 GENTRoute description