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group portrait

 

Prof. Dr. Michael U. Martin

Professor of Immunology

Schubertstraße 81
D-35392 Giessen

Tel.: +49-641-99-34250 Fax: -34259
E-Mail: Michael.Martin@bio.uni-giessen.de
Homepage: http://www.bio.uni-giessen.de/home/immunologie

 

 

 

Scientific Background: 1978-1984 ‘Diplom’ in Biochemistry, University of Hannover / Hannover Medical School, ‘Diplom thesis’, Biochemistry Hannover Medical School (W. Lamprecht / W. Müller); 1984-1986 ‘Doctoral thesis’, Institute of Molecular Pharmacology, Hannover Medical School (Klaus Resch), 1986-1987 Postdoctoral research fellow in the special research program "chronic inflammation" SFB 244 Hannover Medical School, 1987-1989 Head of research laboratory in biotechnology, immunology/oncology, BASF AG, Ludwigshafen, 1989-1990 Guest researcher SFB 244,1990-1991 DFG-funded Postdoctoral research fellow at the Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, (Sir Gustav Nossal / Andrew Boyd), 1992-2002 Senior research fellow and head of research group ‘clinical immunopharmacology’, Institute of Pharmacology (K. Resch) Hannover Medical School, 1994 ‘Habilitation’: venia legendi for ‘Immunology’ (lecturer), Hannover Medical School, 1999 ‘Ausserplanmaessiger Professor’, since 2003 Full Professor of Immunology at the Justus-Liebig-University Giessen.

Cooperations: Werner Falk, University of Regensburg, Germany; Holger Wesche, Tularik Inc. South San Francisco, USA; Diana Boraschi, CNR, Pisa, Italy; Alberto Mantovani, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy; Charles Dinarello, University of Denver, Colorado, USA; Detlef Neumann, Hannover Medical School, Hannover, Germany; Wim van den Berg, University of Nijmegen, The Netherlands

 

Resaerch Groups

 

Signal Transduction Mechanisms of the Toll / Interleukin-1 Receptor Family
The members of the Toll / IL-1 receptor family are alarm receptors in innate and adaptive immunity. They orchestrate acute inflammation in response to challenge with pathogens and guarantee a rapid and effective acute immune reaction. However, unregulated and prolonged triggering of these receptors may participate in acute and chronic inflammatory disorders such as sepsis or rheumatoid arthritis. We are currently investigating the receptor proximal signal transduction events of this receptor family, the type I IL-1 receptor being the proto-type for our studies. We focus on the molecular mechanisms of activation and regulation of the Interleukin-1 receptor associated kinase family members IRAK-1 and IRAK-4. Responsible group leader: Dr. Christian Kollewe


Novel strategies for the intervention in acute and chronic inflammatory disorders
Interleukin-1 (IL-1) is a master pro-inflammatory cytokine. Prolonged and enhanced action of IL-1 causes chronic inflammatory disorders such as rheumatoid arthritis. Therefore, inhibition of IL-1 action is a promising strategy to intervene in chronic inflammation. We identify target structures on different levels of the cell, i.e. the receptor level, or the initial signal transduction machinery, or subsequent amplifying or regulatory steps. We try to unravel the molecular mechanism of action of the individual receptor or signaling components in order to find the best way of interfering with its function. Recently, we developed a recombinant soluble co-receptor for IL-1 which works as a competitive antagonist of IL-1 in vitro and in vivo. We are presently testing different possibilities of inhibiting the receptor most proximal kinases IRAK-4 and IRAK-1 in the signaling cascade of the Toll/ IL-1 receptor family. Responsible group leader: Prof. Dr. Michael Martin


Modulation of the immune response by targeting dendritic cells
Dendritic cells (DC) are probably unique in efficiently activating naive T cells and are regarded as the principal inducers of immune responses. Depending on their activation state, DC can either induce antigen-specific immune responses or antigen-specific tolerance. We investigated differential gene expression accompanied with activation of DC applying Differential Display, differential library screening and microarray analysis and identified numerous differentially expressed genes. The function of some of these molecules including the novel CC chemokine CCL22 and the actin-bundling protein fascin was analyzed in DC in detail and the regulatory elements of the fascin gene were used to establish an expression system that allows for transcriptional targeting of mature DC of mouse and man. Currently we use this approach to express proteins selectively in DC to induce and modulate immune responses in vivo. Responsible group leader:  PD Dr. Ralf Ross

 

Literature:  

 

R.L. Smeets, F.A.J. van de Loo, L.A.B. Joosten, O.J. Arntz, A.B. Bennink, W.A. Loesberg, I.P. Dmitriev, D.T. Curiel, M.U.Martin, W.B. van den Berg (2003) The soluble form of the IL- receptor accessory protein (sIL-1RAcP) is an inhibitor of IL-1, effective in collagen induced arthritis. Arthritis and Rheumatism 2003, 2949-2958

C. Kollewe, A-C. Mackensen, D. Neumann, J. Knop, P. Cao, S. Li, H. Wesche, M.U. Martin (2004) Sequential auto-phosphorylation steps in the Interleukin-1 Receptor-associated Kinase-1 (IRAK-1) regulate its availability as an adapter in IL-1 signaling. J. Biol. Chem. Published on line November 18, (2003) M309251200

M.U. Martin, H. Wesche (2002) Summary and comparison of the signaling mechanisms of the Toll/Interleukin-1 receptor family (Review) Biochim. Biophys. Acta, Special Edition The Molecular Biology of Cytokines, S. Rose-John Editor, 592, 265-280

R. Ross, S. Sudowe, J. Beisner, XL. Ross, I. Ludwig-Portugall, J. Steitz, T. Tüting, J. Knop, A.B. Reske-Kunz (2003) Transcriptional targeting of dendritic cells for gene therapy using the promoter of the cytoskeletal protein fascin. Gene Ther. 10, 1035-40