Libert Unit - Mouse Genetics in Inflammation

Research field: Regulation of inflammation, infection and aging

Group leader: Prof. Dr. Claude Libert

Tel:+32 9 33 13 700  -  Fax:+32 9 221 76 73

Research topic

The inflammatory response is a fundamentally protective, complex and well conserved mechanism. It is actively involved in the induction of immune responses, e.g. against bacterial infection. Several key molecules in inflammation are normally kept under strict control. When this control fails, cytokines such as TNF, interleukins and interferons can cause extensive damage, leading to conditions such as chronic inflammation, sepsis or shock. We are interested in understanding the biology of some of these cytokines (TNF and IFNs), their receptors and their control mechanisms, and in evaluating their therapeutic relevance. The detailed study of the major TNF receptor, TNFRp55 forms an essential focus of our studies. We also focus on the anti-inflammatory mechanism of the glucocorticoid receptor (GR) and how TNF is compromising the function of the GR. We are identifying other potentially protective and harmful molecules and are studying them in mice. Among these are several members of the family of matrix metalloproteinases (MMPs), which contribute to the development of inflammation. Besides a focus on groups of molecules, we also focus our attention on specific systems, such a the liver and small intestines and the choroid plexus. We are studying these molecules and systems in the context of inflammation and infectious diseases and have plenty of relevant mouse models up and running.


Area of expertise

  • Cytokine biology
  • Inflammation models in mice
  • Sepsis models in mice
  • Nuclear receptors
  • Generation of mouse mutants
  • Mapping and cloning traits in mice
  • Genomics and transcriptomics


Fluorescent staining of MMP7 and lysosyme
located in the Paneth cells of the ileum

Selected publications

  1. Vandevyver et al. Glucocorticoid receptor dimerization induces MKP1 to protect against TNF-induced inflammation,
    J Clin Invest 122, 2130, 2012.
  2. Libert et al. The X chromosome in immune functions: when a chromosome makes the difference.
    Nature Rev Immunol 10, 594-604, 2010.
  3. Huys et al. Type-I Interferon drives TNF-induced lethal shock.
    J Exp Med 206, 1873-1882, 2009.
  4. Takahashi et al. IL-17 produced by Paneth cells drives TNF-induced shock.
    J Exp Med 205, 1755-1761, 2008.
    Proc Natl Acad Sci USA 99, 9340-9345, 2002.
  5. Mahieu et al. The wild-derived inbred mouse strain SPRET/Ei is resistant to LPS and defective in IFN-beta production.
    Proc. Natl. Acad. Sci. USA 103, 2292-2297, 2006.
  6. Van Molle et al. HSP70 protects against TNF-induced lethal inflammatory shock.
    Immunity 16, 685-695, 2002.
  7. Wielockx et al. Inhibition of Matrix Metalloproteinases blocks TNF-induced Lethal Hepatitis and apoptosis and allows safe TNF/IFNg antitumor therapy.
    Nature Medicine 7, 1202-1208, 2001.

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