Mechanisms of host-pathogen interaction during chronic infection, inflammation and carcinogenesis
Bild: Susanne Dürr
Our research group is working on the mechanisms of tumor development in the gastrointestinal tract, especially during chronic inflammation elicited by Helicobacter pylori infection in the stomach. Another focus is the deregulation of the Wnt signaling pathway during bacterial infection in the intestine and colon. In parallel, we are interested in identifying targets to develop novel prophylactic approaches and therapeutic strategies for H. pylori infection and stomach cancer.
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- The roles of tissue resident T cells during H. pylori infection and after immunization
- Characterization of CD8+T cell responses during H. pylori infection
- The in-vivo function of gamma-glutamyltransferase, an essential virulence factor of Helicobacter pylori during colonization and immune response
- H. pylori- induced metabolic changes in gastric epithelial cells
- Non-canonical NF-ĸB signaling in H. pylori infection and gastric carcinogenesis
- Helicobacter infection and microbiota-dependent colonic inflammation and pathogenesis (CRC1371)
- H. pylori interaction with CEACAM receptors
- Function of the tumor suppressor RNF43 and gastrointestinal carcinogenesis
- In vivo analysis of mutations of the tumor suppressor RNF43 in colorectal cancer
- Neo-epitopes derived from the mutated tumor suppressor gene RNF43 as targets for T cell therapy in pancreatic cancer (CRC1321)