van Loo Unit - Cellular and Molecular (Patho)physiology

Research Field: Study of in vivo mechanisms of inflammation-driven autoimmune pathology

Group leader: Prof. Dr. Geert van Loo

Tel: +32 9 33 13 761 - Fax: +32 9 221 76 73

Research topic

Our research aims to understand the in vivo mechanisms by which inflammation drives (autoimmune) pathology. For these studies we make use of Cre/LoxP-mediated gene targeting technology allowing tissue-specific gene deletion in mice, in combination with mouse models of human inflammatory diseases. Central in our research is the study of the molecular mechanisms involving NF-κB, apoptosis and ER stress in pathologies such as inflammatory bowel disease, rheumatoid arthritis, diabetes and multiple sclerosis.

Areas of expertise

  • 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

Technology transfer potential

  • Novel mouse models for inflammatory diseases
  • Therapeutic targets in inflammation and autoimmunity

Selected publications

  1. Vande Walle, et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis.
    Nature. 512, 69-73, 2014.
  2. Vereecke, et al. A20 controls intestinal homeostasis through cell-specific activities.
    Nat Comm. 5, 5103, 2014.
  3. Mc Guire C et al. Paracaspase MALT1 deficiency protects mice from autoimmune-mediated demyelination.
    Journal of Immunology, 190, 2896-2903, 2013.
  4. Matmati M et al. A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis. Nature Genetics, 43, 908-912, 2011.
  5. Vereecke L et al. Enterocyte specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis. Journal of Experimental Medicine, 207, 1513-1523, 2010.

Myelinated axons in brain corpus callosum

Mucus produced by intestinal goblet cells preventing bacterial adhesion in the colon

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