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Prof. Dr. Vigo Heissmeyer

Head of Institute of Molecular Immunregulation (AMIR)

"Deciphering the molecular mechanisms that control T cell-driven immune responses will create critical knowledge for future therapies against autoimmune diseases or immune cell therapies against cancer."

Prof. Dr. Vigo Heissmeyer

Head of Institute of Molecular Immunregulation (AMIR)

"Deciphering the molecular mechanisms that control T cell-driven immune responses will create critical knowledge for future therapies against autoimmune diseases or immune cell therapies against cancer."

His academic career started with a PhD in signal transduction at the MDC in Berlin and a Postdoctoral Fellowship at Harvard Medical School in Boston, USA, where he studied transcriptional programs and signal transduction in T helper cells. Returning to Germany and building his own Young Investigator Group at Helmholtz Munich a new focus on post-transcriptional gene regulation by RNA-binding proteins and mRNA modifications was established.

 

His work aims to understand the post-transcriptional gene regulation underlying T cell fate decisions including development, activation, differentiation and formation of effector or memory cells. These programs protect us from invading pathogens and tumor cells but, once dysregulated, can also cause autoimmunity or inflammation.

Mouse models molecular and cellular immunology,biochemistry in primary T cells

2001-2005

Postdoctoral Fellow, Harvard Medical School, Boston, USA

2005-2009

Young Investigator at Helmholtz Munich

2009-2001

Tenured Group leader at the Institute of Molecular Immunology (Helmholtz Munich)

since 2012

Head of Research Unit (Molecular Immune Regulation, Helmholtz Munich) and Professor at the Institute for Immunology (Ludwig-Maximilians-Universität München)

Honors and Awards

2011
ERC starting grant (consolidator category)

Publications by Vigo Heissmeyer

Read more

2022 Scientific Article in Nature Communications

Günsel, G.G. ; Conlon, T.M. ; Jeridi, A. ; Kim, R. ; Ertüz, Z. ; Lang, N.J. ; Ansari, M. ; Novikova, M. ; Jiang, D. ; Strunz, M. ; Gaianova, M. ; Hollauer, C. ; Gabriel, C. ; Angelidis, I. ; Doll, S. ; Pestoni, J. ; Edelmann, S.L. ; Kohlhepp, M.S. ; Guillot, A. ; Bassler, K. ; Van Eeckhoutte, H.P. ; Kayalar, Ö. ; Konyalilar, N. ; Kanashova, T. ; Rodius, S. ; Ballester-Lopez, C. ; Genes Robles, C.M. ; Smirnova, N.F. ; Rehberg, M. ; Agarwal, C. ; Krikki, I. ; Piavaux, B. ; Verleden, S.E. ; Vanaudenaerde, B. ; Königshoff, M. ; Dittmar, G. ; Bracke, K.R. ; Schultze, J.L. ; Watz, H. ; Eickelberg, O. ; Stöger, T. ; Burgstaller, G. ; Tacke, F. ; Heissmeyer, V. ; Rinkevich, Y. ; Bayram, H. ; Schiller, H. B. ; Conrad, M. ; Schneider, R. ; Yildirim, A.Ö.

The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD.