B05 - Cross-talk between innate immunity and extracellular vesicles (EV) forms a checkpoint regulating long-lasting neuroinflammation after brain injury

https://rdp.sfb274.de/ (Research Data Platform) https://gepris.dfg.de/gepris/projekt/408885537 (DFG Gepris entry) The central nervous system (CNS) is a terminally differentiated tissue, where any insult carries a heightened risk - yet the tissue response to these insults is variable and can range from irreversible destruction to almost complete recovery. The rules that instruct these divergent outcomes are still unknown. The aim of this CRC is therefore to understand the biology of the multicellular ...

The oligodendrocyte progenitors (OPCs) are at the front of the glial reaction to the traumatic brain injury. However, regulatory pathways steering the OPC reaction as well as the role of reactive OPCs remain largely unknown. Here, we compared a long-lasting, exacerbated reaction of OPCs to the adult zebrafish brain injury with a timely restricted OPC activation to identify the specific molecular mechanisms regulating OPC reactivity and their contribution to regeneration. We demonstrated that the ...

Traumatic brain injury leads to a highly orchestrated immune- and glial cell response partially responsible for long-lasting disability and the development of secondary neurodegenerative diseases. A holistic understanding of the mechanisms controlling the responses of specific cell types and their crosstalk is required to develop an efficient strategy for better regeneration. Here, we combine spatial and single-cell transcriptomics to chart the transcriptomic signature of the injured male murine ...

We performed gene expression microarray analysis in the whole telencephalon at different time points during the course of regeneration after nostril or skull brain injury

Spatial transcriptomics of the intact and injured mouse cerebral cortex at 3 days post injury (dpi).

Single cell transcriptomics of all cells of the intact and injured mouse cerebral cortex at 3 and 5 days post injury (dpi), in control condition and upon inhibition of the Tlr1/2 and Cxcr3 pathways.