Center for Physiology and Pathophysiology
Institute of Immunology
Lazarettgasse 19
A-1090 Vienna, Austria
phone: + 431 40160 65001
fax:      + 431 40160 965006
Email:herbert.strobl@meduniwien.ac.at
Website: http://www.meduniwien.ac.at/immunologie/strobl/

Research interests

My research focuses on understanding the genetic determinants of human hematopoietic stem cell and dendritic cell differentiation and to alter the properties of these cells for medical applications.

Basic models and techniques: We have established cytokine-dependent serum-free differentiation cultures to generate various subsets of granulo-monocytic (GM) and dendritic cells (DC) from CD34⁺ cord blood progenitor/stem cells in vitro. Additionally, we have developed inducible retroviral vector-based expression systems for performing genetic perturbation studies in progenitor cells as well as in post-mitotic leukocyte subsets generated in vitro. For all projects studies we use advanced multiparameter flow cytometry as well as molecular techniques such as DNA cloning and quantitative real time RT PCR.

Selected publications

Taschner S, Koesters C, Platzer B, Jorgl A, Ellmeier W, Benesch, T, Strobl H. Downregulation of RXRa expression is essential for neutrophil development from granulocyte/monocyte progenitors. Blood, 2007 October 3; (Epub ahead of print)

Jörgl, A., B. Platzer, S. Taschner, L. X. Heinz, B. Höcher, P. M. Reisner, F. Göbel, and Strobl H. Human Langerhans cell activation triggered in vitro by conditionally expressed MKK6 is counter regulated by the downstream effector RelB. Blood 2007; 1;109(1):185-93, Epub 2006 Sep 7.

Göbel, F, Taschner S. Jurkin J, Vaculik C, Richter S, Kneidinger D, Mühlbacher C, Bieglmayer C, Elbe-Bürger A, Strobl H. Reciprocal role of GATA-1 and vitamin D receptor in human myeloid dendritic cell differentiation. Blood. 2009 prepublished online Aug 31. DOI 10.1182/blood-2009-03-210484.

Jurkin J, Schichl YM, Köffel R, Bauer T, Richter S, Konradi S, Gesslbauer B, and Strobl H. miR-146a is differentially expressed by myeloid dendritic cell subsets and desensitizes cells to TLR2-dependent activation. J Immunol. (2010) April 7, online