Dietmar Zehn
Dietmar Zehn
Associate Professor
Humboldt University
Germany
Biography
Dr. Dietmar Zehn is a Group Leader and Born in 1976, Dietmar Zehn earned a MD/PhD degree from the Humboldt University in Berlin in 2004, for having published papers on the antigen presenting capacity of dendritic cells. In the same year, he became a post-doctoral fellow of Michael J. Bevan in the Department of
Immunology at the University of Washington in Seattle, USA. There he investigated how the affinity of T cell receptors (TCR) for self- and foreign-peptide MHC-complexes impacts T cell responses. His key findings are that central and peripheral tolerance routinely fail to eliminate low affinity autoimmune T
cells and that even very low affinity TCR and peptide-MHC interactions are sufficient to generate effector and memory T cells. His excellent expertise in the fields of
immunology of infectious diseases, immunological self-tolerance, and cellular
immunology has led to important scientific contributions. Highlights of his research project is Dietmar Zehn’s scientific interests concentrate on basic and
translational research in molecular and cellular
immunology applied to malignant tumours and infectious diseases. Following up on the notion that immune self-tolerance mechanisms fail to eliminate T
cells that weakly interact with self- or tumorantigens, Dr. Zehn´s research aims to reveal and test novel strategies for utilizing such
cells to eradicate tumours. Using a newly developed research model and a systematic approach he studies which mechanisms normally curtail the tumour-damaging potential of these
cells and he investigates how the restrictions applying to such
cells can be overcome. Furthermore, he focuses on determining cellular and molecular mechanisms controlling T cell expansion and the generation of effector and memory T
cells in acute infections and CD8+ T cell exhaustion during chronic immune responses.
Research Interest
cellular and molecular mechanisms controlling T cell expansion and the generation of effector and memory T cells in acute infections and CD8+ T cell exhaustion during chronic immune responses.
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