Figure 1.

TSPO in astrocytes regulates astrogliosis and severity of autoimmune neuroinflammation.

In multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), cytokines released by infiltrating peripheral immune cells, such as T-cells and macrophages, and activated microglia, and also presence of dying oligodendrocytes cause astrocyte activation and increase in expression of glial fibrillary acidic protein (GFAP). Expression of mitochondrial translocator protein (TSPO) is also upregulated in reactive astrocytes during EAE and MS. Knockout of TSPO in astrocytes reduces reactive astrogliosis, and level of inflammatory mediators in the spinal cord tissue of EAE mice resulting in attenuation of disease clinical symptoms.