Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery Minako Ito, Akihiko Yoshimura Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan
Foxp3+ regulatory T cells (Tregs) are critical components of immune tolerance. In addition, Tregs residing in non-immune tissues perform specialized functions in tissue homeostasis and remodeling. The characteristics and functions of brain Tregs, however, are not well understood, in part because the number of Tregs in the brain under normal conditions is very low. However, during the chronic phase two weeks after ischemic stroke, a massive accumulation of Tregs occurs in the brain. Here we show that the amplification of brain Tregs is dependent on interleukin (IL)-2, IL-33 and T cell receptor (TCR) recognition, and infiltration into the brain is driven by chemokines. Gene expression analysis revealed that brain Tregs related to Tregs in other tissues such as adipose tissue (VAT) and muscle, however, brain Tregs are apparently different from them and express several unique genes related to the nerve system. Brain Tregs suppress astrocyte activation (astrogliosis) and reduce neural damages via the production of amphiregulin (Areg), a low-affinity epidermal growth factor receptor (EGFR) ligand. Stroke is a leading cause of neurological disability, and there is currently no effective method for recovery other than rehabilitation in the chronic phase of cerebral infarction. Our findings suggest that Tregs and their products may provide new therapeutic opportunities for neuronal protection against stroke as well as various other neuroinflammatory diseases.
Credits: None available.
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