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. 2020 Jul 3;13:120. doi: 10.3389/fnmol.2020.00120

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Copyright © 2020 Spampinato, Merlo, Fagone, Fruciano, Sano, Kanda and Sortino.

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/CD4+ reciprocal crosstalk. In Alzheimer’s disease (AD), infiltrating CD4+ cells cross the BBB reaching the glia limitans. Through reciprocal crosstalk, Aβ-exposed astrocytes skew CD4+ towards a Th2 phenotype, inducing the production of IL-4 and BDNF. In the presence of BDNF, Aβ-induced synaptic loss in neurons is prevented. Conversely, in the presence of CD4+ cells, Aβ-exposed astrocytes reduce the release of inflammatory cytokines (IL-6 and IL-1β) and VEGF. As a consequence, endothelial properties at the BBB are preserved.