Zu den Inhalten springen

Institut für Medizinische Mikrobiologie und Hygiene

AG Dr. Tanriver

Dr. med. Yakup Tanriver

Telefon Büro+49 761 203-6522
Telefon Labor+49 761 203-5366
Fax+49 761 203-6562


1994Allgemeine Hochschulreife, Berlin
1994-2001Medizinstudium, Humboldt-Universität, Berlin
1997-2001Studentische Hilfskraft in der Abteilung für Klinische Physiologie, Freie Universität Berlin
2000-2002Medizinische Doktorarbeit unter Leitung von Prof. R. Schindler, Abteilung für Nephrologie und internistische Intensivmedizin, Charité Campus Virchow-Klinikum, Berlin
2002-2005Assistenzarzt, Abteilung für Nephrologie und internistische Intensivmedizin, Charité Campus Virchow-Klinikum, Berlin
2005-2008Post-Doc, Abteilung für Nephrologie und Transplantationsmedizin, Immunoregulation Labaratory (Prof. R. Lechler and Prof. G. Lombardi), King’s College London
2009-2010Assistenzarzt, Abteilung für Nephrologie und Allgemeinmedizin, Universitätsklinikum Freiburg
2010-2012Walter-Hitzig Fellow des Centrums für Chronische Immundefizienz, Universitätsklinikum Freiburg
2012-bis heuteJunior-Gruppenleiter am Institut für Medizinische Mikrobiologie und Hygiene und Assistenzarzt in der Abteilung für Nephrologie und Allgemeinmedizin, Universitätsklinikum Freiburg

Who is who?

Name Postition Telefon E-Mail
Dr. med. Yakup Tanriver AG-Leiter 203-6529 Yakup.Tanriver@uniklinik-freiburg.de
Dr. rer. nat. Jonas Hummel Postdoc 203-6529 jonas.hummel@uniklinik-freiburg.de
Dr. med. Frederic Arnold Postdoc Medizin 203-6529 frederic.arnold@uniklinik-freiburg.de
Nadja Goos MTA 203-6606 nadja.goos@uniklinik-freiburg.de
Lukas Heldman Med. Doktorand 203-6529 lukas.heldmann@uniklinik-freiburg.de
Laurence Kupferschmid Med. Doktorand 203-6529 laurence.kupferschmid@uniklinik-freiburg.de
Benedikt Thelen Med. Doktorand 203-6529 benedikt.thelen@uniklinik-freiburg.de
Bastien Lambert Biol. Doktorand 203-6529 bastien.lambert@uniklinik-freiburg.de


  • C. S. N. Klose, M. Flach, L. Möhle, L. Rogell, T. Hoyler, K. Ebert, C. Fabiunke, D. Pfeifer, V. Sexl, D. Fonseca-Pereira, R. G. Domingues, H. Veiga-Fernandes, S. J. Arnold, M. Busslinger, I. R. Dunay, Y. Tanriver*, and A. Diefenbach*, “Differentiation of Type 1 ILCs from a Common Progenitor to All Helper-like Innate Lymphoid Cell Lineages.,” Cell, vol. 157, no. 2, pp. 340–356, Apr. 2014. *Equally contributing senior-authors
  • Y. Tanriver* and A. Diefenbach, “Transcription factors controlling development and function of innate lymphoid cells.,” Int. Immunol., vol. 26, no. 3, pp. 119–128, Mar. 2014. *Corresponding author
  • I.-M. Pimeisl, Y. Tanriver, R. A. Daza, F. Vauti, R. F. Hevner, H.-H. Arnold, and S. J. Arnold, “Generation and characterization of a tamoxifen-inducible Eomes(CreER) mouse line.,” Genesis, Jul. 2013.
  • L. A. Smyth, K. Ratnasothy, A. Moreau, S. Alcock, P. Sagoo, L. Meader, Y. Tanriver, M. Buckland, R. Lechler, and G. Lombardi, “Tolerogenic Donor-Derived Dendritic Cells Risk Sensitization In Vivo owing to Processing and Presentation by Recipient APCs.,” J. Immunol., vol. 190, no. 9, pp. 4848–4860, May 2013.
  • C. S. N. Klose, E. A. Kiss, V. Schwierzeck, K. Ebert, T. Hoyler, Y. d'Hargues, N. Göppert, A. L. Croxford, A. Waisman, Y. Tanriver*, and A. Diefenbach*, “A T-bet gradient controls the fate and function of CCR6-RORγt+ innate lymphoid cells.,” Nature, vol. 494, no. 7436, pp. 261–265, Feb. 2013. *Equally contributing senior-authors
  • C. S. N. Klose, T. Hoyler, E. A. Kiss, Y. Tanriver, and A. Diefenbach, “Transcriptional control of innate lymphocyte fate decisions.,” Curr. Opin. Immunol., vol. 24, no. 3, pp. 290–296, Jun. 2012.
  • R. Tavaré, P. Sagoo, G. Varama, Y. Tanriver, A. Warely, S. S. Diebold, R. Southworth, T. Schaeffter, R. I. Lechler, R. Razavi, G. Lombardi, and G. E. D. Mullen, “Monitoring of in vivo function of superparamagnetic iron oxide labelled murine dendritic cells during anti-tumour vaccination.,” PLoS ONE, vol. 6, no. 5, p. e19662, 2011.
  • Y. Tanriver, M. J. Betz, L. Nibbe, T. Pfluger, F. Beuschlein, and M. Z. Strowski, “Sepsis and cardiomyopathy as rare clinical manifestations of pheochromocytoma--two case report studies.,” Exp. Clin. Endocrinol. Diabetes, vol. 118, no. 10, pp. 747–753, Nov. 2010.
  • H. Shariff, Y. Tanriver, K. L. Brown, L. Meader, R. Greenlaw, N. Mamode, and S. Jurcevic, “Intermittent antibody-based combination therapy removes alloantibodies and achieves indefinite heart transplant survival in presensitized recipients.,” Transplantation, vol. 90, no. 3, pp. 270–278, Aug. 2010.
  • Y. Tanriver, K. Ratnasothy, R. P. Bucy, G. Lombardi, and R. Lechler, “Targeting MHC class I monomers to dendritic cells inhibits the indirect pathway of allorecognition and the production of IgG alloantibodies leading to long-term allograft survival.,” J. Immunol., vol. 184, no. 4, pp. 1757–1764, Feb. 2010.
  • Y. Tanriver, A. Martín-Fontecha, K. Ratnasothy, G. Lombardi, and R. Lechler, “Superantigen-activated regulatory T cells inhibit the migration of innate immune cells and the differentiation of naive T cells.,” J. Immunol., vol. 183, no. 5, pp. 2946–2956, Sep. 2009.
  • J. Y.-S. Tsang*, Y. Tanriver*, S. Jiang, E. Leung, K. Ratnasothy, G. Lombardi, and R. Lechler, “Indefinite mouse heart allograft survival in recipient treated with CD4(+)CD25(+) regulatory T cells with indirect allospecificity and short term immunosuppression.,” Transpl. Immunol., vol. 21, no. 4, pp. 203–209, Sep. 2009. *Equally contributing first-authors
  • J. Y.-S. Tsang, Y. Tanriver, S. Jiang, S.-A. Xue, K. Ratnasothy, D. Chen, H. J. Stauss, R. P. Bucy, G. Lombardi, and R. Lechler, “Conferring indirect allospecificity on CD4+CD25+ Tregs by TCR gene transfer favors transplantation tolerance in mice.,” J. Clin. Invest., vol. 118, no. 11, pp. 3619–3628, Nov. 2008.
  • J. Tsang, S. Jiang, Y. Tanriver, E. Leung, G. Lombardi, and R. I. Lechler, “In-vitro generation and characterisation of murine CD4+CD25+ regulatory T cells with indirect allospecificity.,” Int. Immunopharmacol., vol. 6, no. 13, pp. 1883–1888, Dec. 2006.
  • R. Schindler, S. G. Tullius, Y. Tanriver, K. Noack, Y. Qun, J.-S. Jürgensen, and U. Frei, “Hypertension increases expression of growth factors and MHC II in chronic allograft nephropathy.,” Kidney Int., vol. 63, no. 6, pp. 2302–2308, Jun. 2003.
  • R. Schindler, Y. Tanriver, and U. Frei, “Hypertension and allograft nephropathy--cause, consequence, or both?,” Nephrol. Dial. Transplant., vol. 15, no. 1, pp. 8–10, Jan. 2000.



The focus of our lab is to understand the role of transcription factors in lymphocyte development and function. Ultimately this analysis will lead to the identification of new regulatory pathways, which can be translated into clinical practice. Thus our lab has a strong interest in basic immunology while at the same time trying to transfer knowledge from “bench to bedside”.  

The developmental program and the effector function of different lymphocyte subsets are determined by transcription factors, which coordinate a regulated program of gene expression. This in turn implicates that the differential expression or the specific combination of transcription factors can serve as a hallmark for different lymphocyte subsets. How transcription factors can have such lineage defining capacity is one of the major challenges in biology.

T-box Transcription

Factors in Innate and Adaptive immunity   NK cells and CD8 T cells are both cytotoxic and efficient cytokine producers upon activation; hence it is reasonable to assume that these functions are controlled by the same set of genes. In fact NK cells and CD8 effector T cells both express high levels of the T-box transcription factors T-bet and Eomesodermin (Eomes) that are defined by their evolutionary highly conserved T-box binding domain. T-bet is the master regulator of T helper 1 cell commitment in CD4 T cells, however primed CD8 T cells from T-bet knockout mice show normal cytotoxicity and IFN-γ production as compared to wild type. In this case Eomes can compensate for T-bet as inhibition of both factors severely impaired cytotoxicity and cytokine production. Similar redundancy has been observed in NK cells from T-bet knockout mice, which show only a modest reduction in cytotoxicity and cytokine production. Nevertheless recent evidence suggests that the two factors are not always interchangeable as T cell specific Eomes knockout mice fail to generate competitive CD8 memory T cells indicating that the two transcription factors also have exclusive targets.

Using transcription factor specific reporter mice in combination with constitutive and conditional knockout mice we want to get a detailed understanding of the spatial and temporal induction of these transcription factors to unravel their distinct roles in different lymphocyte subsets.

FoxP3, Regulatory T Cells (Tregs) and Transplantation Tolerance

 Transplantation has been a very successful approach for the treatment of end stage organ failure and is frequently a life-saving operation. However the necessity for long-term immunosuppression with its myriad toxicities and long-term side effects is one of the major obstacles transplantation medicine faces at the moment.  

The avoidance of any permanent immunosuppression by promoting a state of tolerance could help to increase the number of patients benefiting from this most „physiological“ treatment while at the same time prolonging the survival of transplanted organs. We want to address this challenge by using Tregs. Tregs are defined by the master transcription factor FoxP3. They maintain immunological self tolerance, play a key role in the structural organization of an immune response and myriad attempts have been made to harness their suppressive capacities. We are one of a few labs in the world, which are able to keep regulatory T cells in culture for extended periods (> 12 months). Using different methods to genetically modify these Tregs or to induce them de novo we will test their ability to promote transplantation tolerance in an allo-antigen specific manner.