“Control of metabolic checkpoints by bacterial compounds and their influence on immune cell function”

Tim SPARWASSER, MD
(Institute of Infection Immunology, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Medical School Hannover and the Helmholtz Centre for Infection Research
Hannover, Germany)

Host: Wilfried Ellmeier


Biosketch
Tim Sparwasser is the director of the Institute of Infection Immunology. His research focus lies in host-pathogen interaction with focus on pattern recognition via dendritic cells (DC) and immune regulation through regulatory T cells. Long-term goal of his research work is to understand immune evasion mechanisms of microbial pathogens and development of new approaches to optimize vaccinations. Tim Sparwasser studied human medicine in Mainz (doctor`s degree at the Johannes-Gutenberg-University Mainz), Basel, New York and Munich. As post-doctoral fellow at the Institute of Medical Microbiology (Technical University Munich) he was able to identify bacterial CpG DNA as stimulus for cells of the innate immune system. He received the "Howard Hughes Medical Institute (HHMI) Postdoctoral Fellowship for Physicians" and studied the role of the innate immune system in HIV infection at the HHMI in New York (Skirball Institute, NY University). In 2002 Tim Sparwasser returned to Munich where he established his own research group at the TU Munich. He received his habilitation in Medical Microbiology and completed the board certification in Microbiology and Infection Epidemiology in 2008. Since September 2008 he is Professor for Infection Immunology at Hannover Medical School.

Selected recent publications
•    Puttur et al. (2016) Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. Cell Reports 17(4): 1113 - 1127.
•    Dudek et al. (2016) Lung epithelium and myeloid cells cooperate to clear acute pneumococcal infection. Mucosal Immunol 9(5): 1288-1302.
•    Berod et al., (2014) De novo fatty acid synthesis controls the fate between regulatory T and T helper 17 cells. Nature Medicine, 20(11):1327-33.
•    Mayer et a., Selective and efficient generation of functional Batf3-dependent CD103+ dendritic cells from mouse bone marrow. (2014) Blood, 124(20):3081-91.