Project B06
Disease-overarching mechanisms of Treg-CNS interaction
Background
Acute brain injury in an experimental stroke model leads to pronounced and long-lasting chronic neuroinflammation comparable to chronic neurodegeneration or autoimmune encephalitis mouse models. Both conditions, acute brain injury and autoimmune encephalitis, result in activation of resident microglia, and neuroinflammatory disease progression in both conditions was demonstrated to be critically modulated by Treg cells.
We hypothesize that brain-invading Treg cells are potent modulators of the chronic inflammatory milieu in the injured and recovering brain across a diverse range of brain disorders.
Strategy
We use stroke and experimental autoimmune encephalomyelitis (EAE) models to elucidate the predominant cerebral invasion route for Treg cells, to identify target cells for Treg cells in the chronically inflamed brain, and to decipher the mechanisms by which local Treg cells modulate the cerebral micromilieu.