Prof. Dr. Burkhard Becher

 

Main Goals, Keywords

Our research aims to understand i) the development of tissue-specific autoimmunity ii) the interaction of the nervous system with the immune system under inflammatory conditions:

1) Neuroimmunology, Cytokine biology

2) Identification of pathogenic molecules specific for autoimmune T lymphocytes

3) Immune tolerance and lymphoid development

4) Anti-tumor immunity

Keywords: Autoimmunity, anti-tumor immunity, Neuroimmunology , Neuro-Immune-Networks, Antigen-Presentation, Cytokines, transgenic mice, Gene-targeting, Embryonic stem cells, EAE, MS.

Group Members

1 Professor, 1 Research Associate, 4 Post-docs 2 Research Assistants, 10 PhD-Students.

Previous and Current Research

Although the central nervous system (CNS) has been characterized as an immune privileged site, its privilege can be breached as a result of infection or of the development of anti-self reactivity. In autoimmune diseases such as multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) neuroantigen-reactive, auto-aggressive T lymphocytes escape immune tolerance mechanisms and infiltrate the CNS to cause tissue damage leading to neurologic deficit. A focus of our research is to achieve a better understanding of the events leading to autoimmunity and the pathogenicity of auto-reactive lymphocytes. We further aim to delineate the immune/CNS interface and the ability of CNS-resident cells to orchestrate the development of CNS inflammation.

Techniques and Equipment

In vivo immunology using gene-targeted and transgenic mice, Immune-modulation, protein biochemistry, molecular biology, in vivo bioluminescence imaging, gene-targeting and ES-cell culture.

Selected Publications

• Haak, S., Croxford, A., Kreymborg, K., Heppner, F.L., Pouly, S. Waisman, A* and Becher, B.* 2009 IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation. J.Clin.Invest 119:61-69
• Kreymborg, K., Etzensperger, R., Dumontier, L., Rebollo, A., Haak, S., Heppner, F.L., Renauld, J.C. and Becher, B. 2007 IL-22 is expressed by TH17 cells in an IL-23-dependent fashion, but is not required for the development of EAE J.Immunol. 179:8098-104
• Gutcher, I., Urich, E., Prinz, M., and Becher, B. 2006 IL-18 independent IL-18Rα engagement induces the generation of encephalopathogenic T cells in vivo. Nature Immunol. 7:946-953
• Greter, M., Heppner, F, Lemos, M.P., Odermatt, B.M., Goebels, N., Laufer, T., Noelle, R.J., and Becher, B. 2005  Dendritic cells permit immune invasion of the CNS during experimental autoimmune encephalomyelitis. Nature Med. 11:328-334
• Heppner, F.L., Greter, M., Marino, D., Raivich, G., Prinz, M., Priller, J., Hoevelmeyer, N., Waisman, A., Becher, B., and Aguzzi, A. 2005 Experimental autoimmune encephalomyelitis repressed by microglial paralysis Nature Med. 11:146-52

Funding

Swiss National Research Foundation, Swiss MS-Society, National MS-Society (USA), Koetser Foundation, NCCR Neural Plasticity and Repair, Merck-Serono

URL

www.neuroimmunology.uzh.ch