B05 - Mechanisms and consequences of inflammasome mediated mitochondrial impairment in Mycobacterium tuberculosis infected myeloid cells
Jan Rybniker
Clinic I for internal medicine, University of Cologne
Contact: jan.rybniker(at)uk-koeln.de
For more information visit: Rybniker lab
Abstract
Mycobacterium tuberculosis (Mtb) is a highly successful intracellular pathogen based on its ability to manipulate innate immunity countermeasures of its major host, the human macrophage. Lytic host cell death is essential for bacterial dissemination and represents an important research topic both mechanistically and from a therapeutic perspective. This project aims to study how Mtb modulates regulated cell death in myeloid cells and to address the functional role of different cell death pathways in Mtb infection.
Recent Publications
Simonis A., Theobald S. J., Koch A. E., Mummadavarapu R., Mudler J. M., Andromachi P., Göbel U., Acton R., Winter S., Albus A., Holzmann D., Albert M., Hallek M., Walczak H., Ulas T., Koch M., Tessarz P., Hänsel-Hertsch R., Rybniker J., Persistent epigenetic memory of SARS-CoV-2 mRNA vaccination in monocyte-derived macrophages, Mol Syst Biol (2025), DOI:10.1038/s44320-025-00093-6, MSB-2023-11820