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. 2018 Jul 5;15:197. doi: 10.1186/s12974-018-1241-2

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 10 — The interaction among MCP-1/CCR2 signaling, TLR4, and GSK3β in ethanol-induced neuroinflammation. EtOH may stimulate TLR4 and possibly CCR2, and activate the downstream effectors, such as TRIF and MyD88. Active TLR4 may also activate GSK3β which may further stimulate TLR4 pathway. As a result, the activation of TRIF, MyD88, and GSK3β stimulates transcription factors which upregulate the expression of proinflammatory cytokines and chemokines (e.g., TNF-α, IL6, and MCP-1). The released MCP-1 interacts with CCR2 and further activates TLR4 and GSK3β; the positive feedback loop intensifies the neuroinflammation that is toxic to neurons in the developing CNS