Dominik Aschenbrenner, Postdoctoral Fellow
While performing my diploma studies in Microbiology and Genetics at the University of Vienna, I soon got fascinated by the diversity and complexity of the research field of Immunology. Therefore I chose to focus on studying host-pathogen interaction, vaccinology and adjuvant research for the final stage of my undergraduate studies and my diploma thesis project.
After my graduation in Vienna, I wanted to pursue my interests in life science research while specifically focusing on human T cell immunology, for which I joined the Cellular Immunology group of Dr. Federica Sallusto at the Institute for Research in Biomedicine (IRB) as a doctoral student.
During my time at the IRB and the Swiss federal institute of technology Zürich (ETHZ), I had the great chance to study human T cell differentiation, pathogen specificity, phenotype, and function, in the context of host-pathogen interaction and autoimmunity, at the cellular and molecular level. More specifically, my doctoral studies were focused on the ontogeny of pro- and anti-inflammatory phenotypes of human memory Th17 cells, and the regulation of these diverse functional subclasses on the molecular level. Subsequent to my graduation at the ETHZ I wanted to continue working in the field of host-pathogen interaction and autoimmunity while maintaining a strong focus on human immunology and combining cellular and molecular experimental approaches as well as connecting basic research with clinically translational aspects.
Host-microbe interactions, the regulation of pro-inflammatory immune responses and the phenotypic and functional heterogeneity of immune cells have fascinated me from the beginning of my studies in Microbiology and Genetics at the university of Vienna and continued to be the focus of my doctoral studies in Immunology and Microbiology at the ETH Zurich. Subsequent to my graduation from the ETHZ I joined the Uhlig Group to continue working with a strong focus on human immunology, combining cellular and molecular experimental approaches and connecting basic research with clinically translational aspects.
My research at the Translational Gastroenterology Unit is concentrated to develop a better understanding of immune mechanisms, mediators and cell types that contribute to the pathology of inflammatory bowel disease (IBD).
I am particularly interested in combining rare disease genetics that present with (very) early onset intestinal inflammation with common genetic variation in adult IBD patients to study immune regulation pathways that are critical for the development of IBD and may inform patient stratification and novel treatment strategies for personalized medicine.
- Regulation of cellular sources and production of IL-23 in IBD
- Analysis of genetically identified immune regulation pathways in IBD
- Rare disease genetics and primary immunodeficiency.
Schwerd T, Twigg SRF, Aschenbrenner D, et al. A biallelic mutation in IL6ST encoding the GP130 co-receptor causes immunodeficiency and craniosynostosis. J Exp Med 2017;42:jem.20161810.
Hu D, Notarbartolo S, Croonenborghs T, Patel B, Cialic R, Yang T, Aschenbrenner D, et al. Transcriptional signature of human pro-inflammatory TH17 cells identifies reduced IL10 gene expression in multiple sclerosis. Nat Commun 2017;8(1):1600.
Mele F, Basso C, Leoni C, Aschenbrenner D, et al. ERK phosphorylation and miR-181a expression modulate activation of human memory TH17 cells. Nat Commun 2015;6:6431.
Zielinski CE, Mele F, Aschenbrenner D, et al. Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β. Nature 2012;484(7395):514–8.