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. 2018 Sep 7;9:1930. doi: 10.3389/fimmu.2018.01930

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Copyright © 2018 Ruytinx, Proost, Van Damme and Struyf.

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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CX₃CL1-CX₃CR1 interaction between neurons and microglial cells in the CNS. CX₃CL1 is released from the neurons and interacts with the CX₃CR1 receptor expressed on CNS microglia. CX₃CL1 signaling induces (dashed arrow) a neuroprotective state (A), characterized by the suppressed release of pro-inflammatory cytokines (TNF-α, IL-1β) and upregulation of heme oxygenese 1 (HMOX1). In several murine models of neurodegenerative diseases, genetic deficiency of CX₃CR1 is associated with potentially detrimental secretion of pro-inflammatory cytokines and reactive nitrogen species (NO) causing (dotted arrow) neurotoxicity (B).