A5021593932- NF-κB Signaling Pathways
- Immune Response and Inflammation
- interferon and immune responses
- Cell death mechanisms and regulation
- Inflammasome and immune disorders
- Cytokine Signaling Pathways and Interactions
- Autophagy in Disease and Therapy
- Immunotherapy and Immune Responses
- Immune cells in cancer
- Immune Cell Function and Interaction
- IL-33, ST2, and ILC Pathways
- Ubiquitin and proteasome pathways
- Mitochondrial Function and Pathology
- Autoimmune Bullous Skin Diseases
- Helicobacter pylori-related gastroenterology studies
- Immunodeficiency and Autoimmune Disorders
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- RNA regulation and disease
- Cancer Research and Treatments
- Pulmonary Hypertension Research and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Diabetes and associated disorders
- Cancer Immunotherapy and Biomarkers
- Growth Hormone and Insulin-like Growth Factors
- Urticaria and Related Conditions
VIB-UGent Center for Inflammation Research
2015-2024
Ghent University
2015-2024
Cancer Research Institute Ghent
2021-2024
Ghent University Hospital
2014-2021
Vlaams Instituut voor Biotechnologie
2003-2018
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2012
University of Cologne
2012
Maastricht University
2012
European Bioinformatics Institute
2004-2011
Institute of Molecular Biology and Biophysics
2010
Murine L929 fibrosarcoma cells treated with tumor necrosis factor (TNF) rapidly die in a necrotic way, due to excessive formation of reactive oxygen intermediates. We investigated the role caspases cell death pathway. When cytokine response modifier A (CrmA), serpin-like caspase inhibitor viral origin, was stably overexpressed cells, latter became 1,000-fold more sensitive TNF-mediated death. In addition, TNF sensitization also observed when were pretreated Ac-YVAD-cmk or zDEVD-fmk, which...
Growing up on a dairy farm protects children from allergy, hay fever, and asthma. A mechanism linking exposure to this endotoxin (bacterial lipopolysaccharide)-rich environment with protection has remained elusive. Here we show that chronic low-dose or dust mice developing house mite (HDM)-induced Endotoxin reduced epithelial cell cytokines activate dendritic cells (DCs), thus suppressing type 2 immunity HDMs. Loss of the ubiquitin-modifying enzyme A20 in lung epithelium abolished protective...
A20 is a nuclear factor κB (NF-κB) target gene that encodes ubiquitin-editing enzyme essential for the termination of NF-κB activation after tumor necrosis (TNF) or microbial product stimulation and prevention TNF-induced apoptosis. Mice lacking succumb to inflammation in several organs, including intestine, mutations have been associated with Crohn’s disease. However, ablation activity, specifically intestinal epithelial cells (IECs), promotes inflammation. As deficiency sensitizes...