Rudi Beyaert Lab

Research focus

Dysregulated immune signaling may lead to the development of chronic autoimmune diseases and cancer. The Beyaert group studies the complex role of key signaling molecules in the fine-tuning and self-limiting nature of major signaling pathways that control gene expression in response to inflammatory triggers, further insights of which raises the prospect for better understanding and rational design of therapeutics for several diseases, including autoimmunity, allergy and cancer. The researchers use a variety of omics-based molecular approaches combined with cellular models, mouse gene targeting and mouse models of human disease.

A major research interest of the group is the function and regulation of MALT1. The group’s discovery that MALT1 holds a unique proteolytic activity in lymphocytes has led to a conceptual breakthrough and initiated a strong interest worldwide in the therapeutic targeting of MALT in the context of autoimmunity and certain MALT1-dependent lymphoma cancers. Besides studying the complex role of MALT1 in T cell receptor signaling and T cell homeostasis, the Beyaert lab has taken another great leap forward by also studying the role of MALT1 signalosomes in skin and gut epithelial cells in the context of psoriasis and colitis, respectively.

A second research line focuses on IL-33, a cytokine that is well known for its key role in allergy. Here, the team is studying not only the molecular mechanisms that regulate IL-33 activity, but also uses innovative protein engineering approaches to develop novel IL-33 targeting biologics as new tools to treat allergic and other diseases in which IL-33 plays an important role.

Recently, a third and completely novel research line has been initiated, which aims to investigate the biosynthesis and anti-inflammatory function of two metabolites, abscisic acid and salicylic acid, as novel endogenous immune regulators in mammals.

Finally, Rudi Beyaert also coordinates the recently launched VIB Grand Challenge Program on Primary Immune Deficiency, which is a multidisciplinary translational initiative that addresses the urgent need for molecular diagnostic tools to better identify and classify PID patients and guide therapeutic decisions in the clinic.

Area of expertise

  • Molecular signaling in inflammation and immunity
  • Protein-protein interactions, phosphorylation and ubiquitination
  • Cytokines, Toll-like receptor and T cell receptor signal transduction
  • NF-kappaB signaling
  • Mouse gene targeting and human disease models

Technology transfer potential

  • Novel therapeutic targets in inflammation and cancer (e.g. MALT1)
  • Novel immunomodulatory products (e.g. IL-33 trap)
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Publications

IL-33trap is a novel IL-33-neutralizing biologic that inhibits allergic airway inflammation.Holgado Aurora* Braun Harald* Van Nuffel Elien Detry Sammy Schuijs Martijn Deswarte Kim Vergote Karl Haegman Mira Baudelet Griet Haustraete Jurgen Hammad Hamida Lambrecht Bart Savvides Savvas Afonina Inna° Beyaert Rudi@JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 144, 204-215, 2019* These authors contributed equally° These authors contributed equally@ These authors are corresponding.
MALT1-deletion in T-cells protects against the development of auto-immune arthritis, but causes spontaneous osteoporosis.@Gilis Elisabeth Gaublomme Djoere Staal Jens Venken Koen Dhaenens Maarten Lambrecht Stijn Coudenys Julie Decruy Tine Schryvers Nadia Driege Yasmine Dumas Emilie Demeyer Annelies De Muynck Amélie van Hengel Jolanda Van Hoorebeke Luc Deforce Dieter Beyaert Rudi° @Elewaut DirkArthritis & Rheumatology, , , 2019° These authors contributed equally@ These authors are corresponding.
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 Inna Van Nuffel Elien Baudelet Griet Driege Yasmine Kreike Marja Staal Jens Beyaert RudiEMBO 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

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.

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 71 9052 GENTRoute description