Wienands, Jürgen, Prof. Dr.

Professor of Cellular and Molecular Immunology

  • 1982-89 Study of Biology at the University of Cologne; graduated at the Institute of Genetics, Dept. of Immunology
  • 1989-92 Ph.D. poject at the Max Planck Institute for Immunobiology, Freiburg, Germany
  • 1992-94 Postdoctoral fellow at the Dept. of Preclinical Research at Sandoz Pharma Ltd., Basel, Switzerland
  • 1994-96 Postdoctoral fellow at the Max Planck Institute for Immunobiology, Freiburg, Germany
  • 1996-2001 Group leader at the University of Freiburg, Institute of Biology III
  • 2001 "Habilitation" and Venia Legendi in "Molecular Immunology and Biochemistry"
  • 2001-2004 Full Professor for "Biochemistry and Molecular Immunology" at the University of Bielefeld
  • since August 2004 Full Professor for "Molecular and Cellular Immunology" at the University of Göttingen
  • 2015-2016 President of the German Society for Immunology (DGfI)
  • 2012-2016 Member of the DFG Review Panel Section 201 (Basic Research in Biology and Medicine) of the German Research Foundation DFG (Deutsche Forschungsgemeinschaft)
  • since 2016: Member of the DFG Review Panel Section 204 (Microbiology, Virology, Immunology) of the German Research Foundation DFG (Deutsche Forschungsgemeinschaft)
  • since 04/2020: Dean of Research of the University Medical Center Göttingen

  • Major Research Interests
    The signature structure of B lymphocytes is their clonotypic antigen receptor (BCR), which recognizes extracellular pathogens or toxins, and consequently initiates their combating by soluble antibodies. Our research focuses on how the ligated BCR activates intracellular signaling pathways upon primary and secondary antigen encounter. Our studies showed that BCR classes expressed on antigen-experienced, so-called memory B cells, possess a signal amplification mechanism that lowers the BCR signaling threshold compared to newly generated B cells. This finding provides a molecular explanation for immunological memory which is the fundamental basis for successful vaccination strategies. We also identified key effector proteins of the BCR such as SLP-65 or CIN85. They function as adaptor proteins which nucleate the formation of multi-molecular protein complexes to integrate and amplify BCR signals. Interference with expression or function of these effectors cause severe immunodeficiencies in mouse and man. To investigate these processes we apply cutting edge technologies of biochemistry and genetics including protein interaction studies, flow cytometry, targeted gene disruption in cell culture and embryonic stem cells followed by reconstitution experiments using electroporation techniques or retroviral gene transfer.

    Homepage Department/Research Group:

    Selected Recent Publications
  • Keller B, Shoukier M, Schulz K, Bhatt A, Heine I, Strohmeier V, Speckmann C, Engels N, Warnatz K, Wienands J (2018) Germline deletion of CIN85 in humans with X chromosome-linked antibody deficiency. J Exp Med. 215(5): 1327-1336
  • Kühn J, Wong LE, Pirkuliyeva S, Schulz K, Schwiegk C, Fünfgeld KG, Keppler S, Batista FD, Urlaub H, Habeck M, Becker S, Griesinger C, Wienands J (2016) The adaptor protein CIN85 assembles intracellular signaling clusters for B cell activation. Sci Signal 9(434): ra66
  • Lutz J, Dittmann K, Bösl MR, Winkler TH, Wienands J, Engels N (2015) Reactivation of IgG-switched memory B cells by BCR-intrinsic signal amplification promotes IgG antibody production. Nat Commun 6: 8575
  • Engels N, König LM, Schulze W, Radtke D, Vanshylla K, Lutz J, Winkler TH, Nitschke L, Wienands J (2014) The immunoglobulin tail tyrosine motif upgrades memory-type BCRs by incorporating a Grb2-Btk signalling module. Nat Commun 5: 5456

  • for review see:
  • Wienands J, Engels N (2016) The Memory Function of the B Cell Antigen Receptor. Curr Top Microbiol Immunol 393: 107-21