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Marc Schmidt-Supprian - Immunopathologie und Signal Transduction
Our immune system protects us against invasion by foreign pathogens, such as bacteria, viruses and parasites. However, we pay an evolutionary price for our highly efficient and sophisticated immune defense, namely immunopathology. Immunopathologies include exaggerated responses to harmless substances, also termed allergic responses, misguided responses against our own body, which can lead to autoimmune diseases and the uncontrolled expansion of immune cells, which in turn can cause cancer.
The Schmidt-Supprian research group investigates the molecular and cellular mechanisms underlying such disorders. Immune cells can identify foreign microbial components through a host of cell surface receptors. These receptors then relay signals to the nucleus, where transcription factors activate the expression of genes whose protein products help fight the invaders. Misguidance of such signal transduction events can result in autoimmunity and leukemia or lymphomas, the most prevalent cancers of the immune system. To study critical mechanisms of immunopathology, the group employs genetic loss and gain of function approaches in the mouse combined with cellular and biochemical approaches. Within the immune systems, the main focus is on B and T lymphocytes and mast cells. In these cells, we investigate the regulation of genes and proteins whose exaggerated functions or malfunctions directly contribute to immunpathologies.
Marc Schmidt-Supprian studied chemistry and biochemistry at the Universities of Würzburg and Tübingen and Trinity College Dublin. Between 1999 and 2003 he completed his doctoral studies under the supervision of Klaus Rajewsky at the University of Cologne and Harvard Medical School in Boston, acquiring his doctorate in 2003. He continued to work with Klaus Rajewsky at Harvard as a postdoctoral fellow (2004) and as a junior investigator / instructor in pathology (2004 – 2007). At the end of 2007, Marc Schmidt-Supprian started a DFG Emmy Noether research group at the Max Planck Institute of Biochemistry in Martinsried. In 2014 he was appointed to a tenure track professorship at the School of Medicine of the Technical University Munich. Since 2019 he is director of the institute of experimental hematology.
- Consolidator Grant from the European Research Council (2015)
- Heisenberg Fellowship from the German Research Foundation, DFG (2012)
- Emmy Noether Program from of the German Research Foundation, DFG (2007)
Bortoluzzi, S., Dashtsoodol, N., Engleitner, T., Drees, C., Helmrath, S., Mir, J., Toska, A., Flossdorf, M., Ollinger, R., Solovey, M., Colome-Tatche, M., Kalfaoglu, B., Ono, M., Buch, T., Ammon, T., Rad, R., Schmidt-Supprian, M. (2021). Brief homogeneous TCR signals instruct common iNKT progenitors whose effector diversification is characterized by subsequent cytokine signaling. Immunity.
Kober-Hasslacher, M., Oh-Strauss, H., Kumar, D., Soberon, V., Diehl, C., Lech, M., Engleitner, T., Katab, E., Fernandez-Saiz, V., Piontek, G., Li, H., Menze, B., Ziegenhain, C., Enard, W., Rad, R., Bottcher, J.P., Anders, H.J., Rudelius, M., Schmidt-Supprian, M. (2020). c-Rel gain in B cells drives germinal center reactions and autoantibody production. J Clin Invest 130, 3270-3286.
Drees, C., Vahl, J.C., Bortoluzzi, S., Heger, K.D., Fischer, J.C., Wunderlich, F.T., Peschel, C., Schmidt-Supprian, M. (2017). Roquin Paralogs Differentially Regulate Functional NKT Cell Subsets. J Immunol 198, 2747-2759.
Vahl, J. C., Drees, C., Heger, K., Heink, S., Fischer, J. C., Nedjic, J., Ohkura, N., Morikawa, H., Poeck, H., Schallenberg, S., Riess, D., Hein, M. Y., Buch, T., Polic, B., Schonle, A., Zeiser, R., Schmitt-Graff, A., Kretschmer, K., Klein, L., Korn, T., Sakaguchi, S. and Schmidt-Supprian, M. (2014). Continuous T cell receptor signals maintain a functional regulatory T cell pool. Immunity 41, 722-736.
Heger, K., Fierens, K., Vahl, J. C., Aszodi, A., Peschke, K., Schenten, D., Hammad, H., Beyaert, R., Saur, D., van Loo, G., Roers, A., Lambrecht, B. N., Kool, M., and Schmidt-Supprian, M. (2014). A20-deficient mast cells exacerbate inflammatory responses in vivo. PLoS biology 12, e1001762.
Vahl, J. C., Heger, K., Knies, N., Hein, M. Y., Boon, L., Yagita, H., Polic, B., and Schmidt-Supprian, M. (2013). NKT cell-TCR expression activates conventional T cells in vivo, but is largely dispensable for mature NKT cell biology. PLoS biology 11, e1001589.
Bertossi, A., Aichinger, M., Sansonetti, P., Lech, M., Neff, F., Pal, M., Wunderlich, F. T., Anders, H. J., Klein, L., and Schmidt-Supprian, M. (2011). Loss of Roquin induces early death and immune deregulation but not autoimmunity. The Journal of experimental medicine 208, 1749-1756.
Chu, Y., Vahl, J. C., Kumar, D., Heger, K., Bertossi, A., Wojtowicz, E., Soberon, V., Schenten, D., Mack, B., Reutelshofer, M., Beyaert, R., Amann, K., van Loo, G., and Schmidt-Supprian, M. (2011). B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause inflammation and autoimmunity in aged mice. Blood 117, 2227-2236.
Sasaki, Y., Calado, D. P., Derudder, E., Zhang, B., Shimizu, Y., Mackay, F., Nishikawa, S., Rajewsky, K., and Schmidt-Supprian, M. (2008). NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells. Proceedings of the National Academy of Sciences of the United States of America 105, 10883-10888.
Sasaki, Y., Derudder, E., Hobeika, E., Pelanda, R., Reth, M., Rajewsky, K., and Schmidt-Supprian, M. (2006). Canonical NF-kappaB activity, dispensable for B cell development, replaces BAFF-receptor signals and promotes B cell proliferation upon activation. Immunity 24, 729-739.