Our research aims to understand the in vivo mechanisms by which inflammation drives (autoimmune) pathology. One major focus concerns the transcription factor NF-κB and the molecular mechanisms by which NF-κB controls inflammatory and apoptotic responses in vivo. Also ER stress and autophagy are being studied in this context, since more and more evidence indicates that also these pathways may be crucially involved in inflammatory reactions and the development of inflammatory pathology. For these studies we use transgenic mice as a model to study gene function in vivo, both through Cre/LoxP-mediated gene targeting allowing tissue-specific gene deletion, and through CRISP/Cas technology to introduce specific mutations in vivo. These mice are characterized in several mouse models of chronic inflammatory pathology, including models for inflammatory bowel disease, rheumatoid arthritis, diabetes, and multiple sclerosis.

• ER stress and NF-κB signaling
• In vivo mouse gene targeting and development of mouse models of inflammatory disease
• Study of the molecular interplay between NF-κB, ER stress and autophagy in tissue homeostasis and inflammatory disease development

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   Nature Immunology, 381-387, 21, 2020.
2. Verboom L, et al. OTULIN Prevents Liver Inflammation and Hepatocellular Carcinoma by Inhibiting FADD- and RIPK1 Kinase-Mediated Hepatocyte Apoptosis.
   Cell Reports, 2237-2247.e6, 30, 2020.
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   Cell Reports, 2689-2701.e4, 29, 2019.
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   Nature Cell Biology, 21, 731-742, 2019.
5. Vande Walle, L et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis.
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