Further Info
By studying how cell death shapes inflammation, metabolism, and tumorigenesis, we seek to advance fundamental knowledge and open new avenues for therapy.
Cell Death and Inflammation in Health and Disease
Our Research
Programmed cell death is essential for normal development, immune balance, and defense against pathogens. However, when dysregulated, it can drive chronic inflammation, tissue damage, autoimmunity, and cancer. Our research explores how different forms of cell death shape immune responses and disease progression — and how these processes can be therapeutically reprogrammed.
The rapid development of novel genome editing strategies is transforming the field of biomedical research and its applications at a breakneck pace. We cover the area of biomedical genome editing with innovative research topics in the areas of cancer therapy, the treatment of genetic diseases, and regenerative medicine.
Research areas
Ageing, metabolic disease, inflammation-associated cancer, ubiquitination, apoptosis, necroptosis, pyroptosis, cellular signalling, signal transduction, post-translational protein modification, inflammation, immunology, innate immunity.
Sensing Danger
Cells detect danger through damage- and pathogen-associated molecular patterns (DAMPs and PAMPs), which activate pattern-recognition receptors (PRRs). This triggers inflammatory cytokines such as TNF, IL-1β, and type I interferons — key mediators of innate immunity.
TNF Signaling, Cell Death and Immunity
Binding of TNF to its receptor TNFR1 can lead to:
- Recruitment of the linear ubiquitin chain assembly complex (LUBAC)
- Cell survival and inflammation via NF-κB/MAPK activation (LUBAC, cIAP1/2)
- Apoptosis through FADD/RIPK1/caspase-8 and necroptosis via RIPK1, RIPK3, and MLKL
- Cell death plasticity: these cell death pathways can interact with mitochondria or nuclei acid sensors, thereby modulating intrinsic cell death responses, metabolism and innate immune signalling
Our research interests
- Linear ubiquitination as a metabolic safeguard mechanism during obesity
- Polyglucosan body diseases caused by genetic alteration in LUBAC components
- Cell death, autophagy and epigenetics in ageing-associated diseases
- Apoptosis – Pyroptosis interaction in solid cancer
- Genetically engineered mouse models to study interactions at the cellular and organ level
- Advanced imaging, molecular, and cell biology techniques to dissect underlying mechanisms
- Therapeutics: towards gene therapy and targeted drug delivery
Contact
Nieves Peltzer
Jun.- Prof. Dr.Director of the Department Genome Editing