Dr. Sven Mostböck 

Institut für Immunologie, Universität Regensburg
F.-J.-Strauss-Allee 11
93042 Regensburg
E-mail: sven.mostboeck@klinik.uni-regensburg.de
Tel: +49 941 944 5466  
Fax: +49-941-944-5462

Research interests

  • T cell function
  • Induction and regulation of T cell responses
  • Interaction of immune system and tumor tissue

Models and techniques

  • mouse models for sepsis and tumor research
  • cellular immunology, especially flow cytometry

Research overview

 

T cell function is tightly regulated in the course of an immune response. First, antigen presenting cells aim at activating a broad spectrum of naïve T cells. A number of costimulatory factors, encompassing membrane bound receptors and soluble cytokines, further enhance the activation status of naïve T cells and allow even T cells of low specificity to react against the invading pathogen. This approach of broad specificity in naïve T cell responses enables the immune system to build an adaptive immune response against a wide variety of pathogens even with a repertoire of low affinity T cells. However, this T cell response needs to be regulated later in the immune response, when the pathogen challenge is declining and strong T cell activity might result in immunopathology.

In sepsis, the bacteria invading the host induce a strong immune reaction that results in bacterial clearance. Interestingly, this immune reaction is followed by a phase of immune suppression, during which the host is more susceptible to subsequent infections. We have also shown that immunization during that phase leads to lower levels of antigen-specific antibodies. Currently, we study the effect of sepsis on subsequent T cell responses and the mechanisms behind possible alterations in T cell function. One candidate mechanism is the activation of the TNF system with its two receptors. Previous studies have shown that TNFR2-deficient mice have an altered reaction towards sepsis as they do not express an immunosuppressive phase. The possible impact of TNF and especially the activation TNFR2 on T cell responses is therefore another focus in our ongoing research.

 

Graduate students

  • Simon Kapustij, Master's degree
  • David Scheureck, Master's degree
  • Konstantin Molitor, medical degree
  • Sabine Weber, medical degree

 

Technical Assistance

  • Karin Holz, histology
  • Anne Pietryga-Krieger, molecular biology
  • Dorothea Weber-Steffens, cell culture

 

 

Publications (last five years)

 

•  Pfeifer, E., J. Polz, D. N. Männel, and S. Mostböck. 2012. Inflammation augments the development of experimental glomerulonephritis by accelerating proteinuria and enhancing mortality. Eur Cytokine Netw 23: 12-14.

•  Pfeifer, E., J. Polz, S. Grießl, S. Mostböck, T. Hehlgans, and D. N. Männel. 2012. Mechanisms of immune complex-mediated experimental glomerulonephritis: possible role of the balance between endogenous TNF and soluble TNF receptor type 2. Eur Cytokine Netw 23: 15-20.

•  Mohr, A., J. Polz, E. M. Martin, S. Grießl, A. Kammler, C. Pötschke, A. Lechner, B. M. Bröker, S. Mostböck, and D. N. Männel. 2012. Sepsis leads to a reduced antigen-specific primary antibody response. Eur J Immunol 42: 341-352.

•  Roesler, E., R. Weiss, E. E. Weinberger, A. Fruehwirth, A. Stoecklinger, S. Mostböck, F. Ferreira, J. Thalhamer, and S. Scheiblhofer. 2009. Immunize and disappear-safety-optimized mRNA vaccination with a panel of 29 allergens. J Allergy Clin Immunol 124: 1070-7.e1-11.

•  di Bari, M. G., M. E. Lutsiak, S. Takai, S. Mostböck, B. Farsaci, R. T. Semnani, L. M. Wakefield, J. Schlom, and H. Sabzevari. 2009. TGF-beta modulates the functionality of tumor-infiltrating CD8+ T cells through effects on TCR signaling and Spred1 expression. Cancer Immunol Immunother 58: 1809-1818.

•  Mostböck, S.. 2009. Cytokine/Antibody complexes: an emerging class of immunostimulants. Curr Pharm Des 15: 809-825.

•  Brewig, N., A. Kissenpfennig, B. Malissen, A. Veit, T. Bickert, B. Fleischer, S. Mostböck, and U. Ritter. 2009. Priming of CD8+ and CD4+ T cells in experimental leishmaniasis is initiated by different dendritic cell subtypes. J Immunol 182: 774-783.

•  Remondo, C., V. Cereda, S. Mostböck, H. Sabzevari, A. Franzusoff, J. Schlom, and K. Y. Tsang. 2009. Human dendritic cell maturation and activation by a heat-killed recombinant yeast (Saccharomyces cerevisiae) vector encoding carcinoembryonic antigen. Vaccine 27: 987-994.

•  Semnani, R. T., P. G. Venugopal, C. A. Leifer, S. Mostböck, H. Sabzevari, and T. B. Nutman. 2008. Inhibition of TLR3 and TLR4 function and expression in human dendritic cells by helminth parasites. Blood 112: 1290-1298.

•  Mostböck, S., M. E. Lutsiak, D. E. Milenic, K. Baidoo, J. Schlom, and H. Sabzevari. 2008. IL-2/anti-IL-2 antibody complex enhances vaccine-mediated antigen-specific CD8+ T cell responses and increases the ratio of effector/memory CD8+ T cells to regulatory T cells. J Immunol 180: 5118-5129.

•  Bernstein, M. B., M. Chakraborty, E. K. Wansley, Z. Guo, A. Franzusoff, S. Mostböck, H. Sabzevari, J. Schlom, and J. W. Hodge. 2008. Recombinant Saccharomyces cerevisiae (yeast-CEA) as a potent activator of murine dendritic cells. Vaccine 26: 509-521.

•  Mostböck, S., S. Vidal, J. Schlom, and H. Sabzevari. 2007. Enhanced levels of costimulation lead to reduced effector/memory CD8+ T cell functionality. J Immunol 179: 3524-3534.

•  Mostböck, S., M. Catalfamo, Y. Tagaya, J. Schlom, and H. Sabzevari. 2007. Acquisition of antigen presentasome (APS), an MHC/costimulatory complex, is a checkpoint of memory T-cell homeostasis. Blood 109: 2488-2495.

 

 

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