Marc Schmidt-Supprian – Immunopathology and signal transduction

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 TUM.

Research focus

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 leukemias 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. 


  • 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)

Key publications

Vahl JC, Drees C, Heger K, Heink S, Fischer JC, Nedjic J, Ohkura N, Morikawa H, Poeck H, Schallenberg S, Rieß D, Hein MY, Buch T, Polic B, Schönle A, Zeiser R, Schmitt-Gräff A, Kretschmer K, Klein L, Korn T, Sakaguchi S, Schmidt-Supprian M, Continuous T-cell receptor signals maintain a functional regulatory T-cell pool, Immunity 41, 722–736 (2014).

Heger K, Fierens K, Vahl JC, Aszodi A, Peschke K, Schenten D, Hammad H, Beyaert R, Saur D, van Loo G, Roers A, Lambrecht BN, Kool M, Schmidt-Supprian M, A20-defi cient mast cells exacerbate infl ammatory responses in vivo, PLoS Biol 12(1):e1001762 (2014).

Vahl JC, Heger K, Knies N, Hein MY, Boon L, Yagita H, Polic B, Schmidt-Supprian M, NKT cell-TCR expression activates conventional T cells in vivo, but is largely dispensable for mature NKT cell biology, PLoS Biol 11(6):e1001589 (2013).

Bertossi A, Aichinger M, Sansonetti P, Lech M, Neff F, Pal M, Wunderlich FT, Anders HJ, Klein L, Schmidt-Supprian M, Loss of Roquin induces early death and immune deregulation but not autoimmunity, J Exp Med 208(9):1749–1756 (2011).

Chu Y, Vahl JC, Kumar D, Heger K, Bertossi A, Wójtowicz E, Soberon V, Schenten D, Mack B, Reutelshöfer M, Beyaert R, Amann K, van Loo G, Schmidt-Supprian M, B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause infl ammation and autoimmunity in aged mice, Blood 117(7):2227–2236 (2011).