Research Group Weih/Hänold
NF-κB-Induced Autoimmunity as Reason for Inflammatory Aging
Medullary thymic epithelial cells (mTECs) are important for t-cells to develop a self-tolerance. As of now, it was assumed that only the alternative NF-κB signaling pathway is necessary to generate these cells. However, our research with mice shows that for this important molecular mechanism both pathways are needed: they have to intercommunicate to create mTEC cells. If this communication is somehow disturbed, our mice develop an autoimmunity characterized by a chronic hepatitis. We hypothesize that autoimmunity is a relevant trigger for so-called inflammatory aging in mice.
Immune Cells in Brain
In cooperation projects with neurobiologists, we want to elucidate the reasons for autoimmune inflammatory processes in the nervous system (neuroinflammation). Recently, we could show that several types of myeloid cells display a high expression of RelB, a transcription factor activated by the alternative signaling pathway of NF-κB. Among these cells are microglia cells, the “immune cells of brain”. With new genetic tools we are able to switch off RelB in myeloid dendritic and microglia cells. By this, we can analyze the role of the alternative NF-κB signaling pathway for neuroinflammation.
The Aging Brain
Further, we lay a strong research focus on neuro-immunological studies of NF-κB’s role in the injured and aged brain. Both NF-κB signaling pathways have important regulatory functions in nerve and glial cells. Together with researchers from Heidelberg, we could show that after stroke the activation of the classical NF-κB signaling pathway in mice leads to loss of nerve cells. Moreover, injured nerve cells can regenerate worse if NF-κB-subunit RelA is active (activated by the classical NF-κB signaling pathway). In contrast, subunit p50 (activated classically as well) is essential for the survival and the regeneration of injured nerve fibers. We now aim at elucidating how the manipulation of RelA and p50 affect the brain’s plasticity – a research project granted by Swizz Velux Foundation. Eventually, we want to come up with findings that help to improve the brain functionality in older age and to slow down degeneration processes like senile dementia.
|Ronny Hänold||+49 3641 email@example.com||Postdoc|
|Marc Riemann||+49 3641 firstname.lastname@example.org||Postdoc|
|Christian Engelmann||+49 3641 email@example.com||Doctoral Student|
|Heike Dittmar||+49 3641 firstname.lastname@example.org||Technical Assistant|
|Swen Hartfielemail@example.com||Master Student|