Ito M, Komai K, Mise-Omata S, Iizuka-Koga M, Noguchi Y, Kondo T, Sakai R, Matsuo K, Nakayama T, Yoshie O, Nakatsukasa H, Chikuma S, Shichita T, Yoshimura A. Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery. Nature. 2019 Jan 2; PubMed.
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University of Southern California
The authors propose an intriguing mechanism for T regulatory cell (Treg) involvement in tissue repair after brain injury. In this detailed report, Yoshimura and coworkers demonstrate Treg amplification dependent on interleukins-2 and -33, serotonin, and T cell receptor. Strikingly, they show that infiltration of Tregs into the ischemic brain is driven by the chemokines CCL1 and CCL20. In the absence of CNS Treg recruitment, astrogliosis and neurotoxicity become exacerbated in the middle cerebral artery occlusion stroke model. This report offers an insightful framework for how adaptive immunity in the form of Tregs referees immune function within the ischemic brain. Could this mechanism also operate in the context of AD? Quite possibly—investigating interaction(s) between Tregs, and perhaps other T cell subsets and amyloid-β/tau pathology, is clearly warranted.
View all comments by Terrence TownKeio University School of Medicine
Thank you for your comments. We have already confimed that Tregs in the brains of AD model mice show brain Treg phenotypes. However, we are not sure whether brain Tregs in AD are good or bad for disease symptoms.
View all comments by Akihiko YoshimuraMake a Comment
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