Head of Institute of Molecular Immunregulation (AMIR)
Prof. Dr. Vigo Heissmeyer
"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."
Academic pathway
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.
Skills & Expertise
Mouse models molecular and cellular immunology, biochemistry in primary T cells
CV
Head of Research Unit (Molecular Immune Regulation, Helmholtz Munich) and Professor at the Institute for Immunology (Ludwig-Maximilians-Universität München)
Tenured Group leader at the Institute of Molecular Immunology (Helmholtz Munich)
Young Investigator at Helmholtz Munich
Postdoctoral Fellow, Harvard Medical School, Boston, USA
Publications by Vigo Heissmeyer
Kübelbeck, T. ; Wichmann, N. ; Raj, T. ; Raj, C. ; Ohnmacht, C. ; Hövelmeyer, N. ; Kramer, D. ; Heissmeyer, V.
Regulation and function of the atypical IκBs-Bcl-3, IκBNS, and IκBζ-in lymphocytes and autoimmunity.Mishima, E. ; O'Neill, T.J. ; Hoefig, K.P. ; Chen, D. ; Behrens, G. ; Henkelmann, B. ; Ito, J. ; Nakagawa, K. ; Heissmeyer, V. ; Conrad, M. ; Krappmann, D.
MALT1 inhibitor MI-2 induces ferroptosis by direct targeting of GPX4.Xu, M. ; Ito-Kureha, T. ; Kang, H.-S. ; Chernev, A. ; Raj, T. ; Hoefig, K.P. ; Hohn, C. ; Giesert, F. ; Wang, Y. ; Pan, W. ; Ziętara, N. ; Straub, T. ; Feederle, R. ; Daniel, C. ; Adler, B. ; König, J. ; Feske, S. ; Tsokos, G.C. ; Wurst, W. ; Urlaub, H. ; Sattler, M. ; Kisielow, J. ; Wulczyn, F.G. ; Łyszkiewicz, M. ; Heissmeyer, V.
Correction to "The thymocyte-specific RNA-binding protein Arpp21 provides TCR repertoire diversity by binding to the 3'-UTR and promoting Rag1 mRNA expression".Bataclan, M. ; Leoni, C. ; Moro, S.G. ; Pecoraro, M. ; Wong, E.H. ; Heissmeyer, V. ; Monticelli, S.
Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Xu, M. ; Ito-Kureha, T. ; Kang, H.-S. ; Chernev, A. ; Raj, T. ; Hoefig, K.P. ; Hohn, C. ; Giesert, F. ; Wang, Y. ; Pan, W. ; Ziętara, N. ; Straub, T. ; Feederle, R. ; Daniel, C. ; Adler, B. ; König, J. ; Feske, S. ; Tsokos, G.C. ; Wurst, W. ; Urlaub, H. ; Sattler, M. ; Kisielow, J. ; Wulczyn, F.G. ; Łyszkiewicz, M. ; Heissmeyer, V.
The thymocyte-specific RNA-binding protein Arpp21 provides TCR repertoire diversity by binding to the 3'-UTR and promoting Rag1 mRNA expression.Chang, Y. ; Bach, L. ; Hasiuk, M. ; Wen, L. ; Elmzzahi, T. ; Tsui, C. ; Gutiérrez-Melo, N. ; Steffen, T. ; Utzschneider, D.T. ; Raj, T. ; Jost, P.J. ; Heink, S. ; Cheng, J. ; Burton, O.T. ; Zeiträg, J. ; Alterauge, D. ; Dahlström, F. ; Becker, J.C. ; Kastl, M. ; Symeonidis, K. ; van Uelft, M. ; Becker, M. ; Reschke, S. ; Krebs, S. ; Blum, H. ; Abdullah, Z. ; Paeschke, K. ; Ohnmacht, C. ; Neumann, C. ; Liston, A. ; Meissner, F. ; Korn, T. ; Hasenauer, J. ; Heissmeyer, V. ; Beyer, M. ; Kallies, A. ; Jeker, L.T. ; Baumjohann, D.
TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf.Schmidt, H. ; Raj, T. ; O´Neill, T.J. ; Muschaweckh, A. ; Giesert, F. ; Negraschus, A. ; Hoefig, K.P. ; Behrens, G. ; Esser, L. ; Baumann, Christina ; Feederle, R. ; Plaza-Sirvent, C. ; Geerlof, A. ; Gewies, A. ; Isay, S.E. ; Ruland, J. ; Schmitz, I. ; Wurst, W. ; Korn, T. ; Krappmann, D. ; Heissmeyer, V.
Unrestrained cleavage of Roquin-1 by MALT1 induces spontaneous T cell activation and the development of autoimmunity.