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. 2019 Jun 11;10:1314. doi: 10.3389/fimmu.2019.01314

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Copyright © 2019 Priego and Valiente.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Astrocytes and acquired immunity. (A) Ischemia induces the production of CCL1/CCL20/Serotonin that attracts T regulatory cells. Once in the brain, Tregs increase their numbers activated by IL-2 and IL-33 and produce AREG that reduces the neuronal damage by impairing STAT3 activity in astrocytes. (B) Treatment with an anti-CD3 blocking antibody intranasally stimulates the production of a subpopulation of T regulatory cells producers of IL-10 at the cervical lymph-nodes. After reaching the brain these cells are responsible for decreasing the expression of genes linked to the pathology by activating the IL-10 receptor in astrocytes. (C) Infiltrating CD8+ T cells are exposed to immune checkpoint ligands and an immunosuppressive secretome generated by pSTAT3+ reactive astrocytes that surround established metastasis. (D) In contrast, pSTAT3- reactive astrocytes produce IL-15 that binds to NKG2D leading to their increased activation and destruction of myelin.