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. 2019 May 17;16:102. doi: 10.1186/s12974-019-1502-8

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© The Author(s). 2019

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. 2 — Hypothetical model for fatigue. Danger signals activate astroglia to produce and release S100B that bind to TLR4 and RAGE receptors on microglia. Activated microglia produce IL-1β that bind specific receptors (IL-1R1/IL-1RAcPb) on neurons and induce sickness behavior. There are no specific receptors for IL-6 that can modulate neurons in the same manner as for IL-1β, but higher levels of IL-6 may through stimulation of TNFα synthesis reduce the amount of Hcrt-1 in neurons. Low levels of Hcrt-1 can lead to or modulate fatigue through unknown pathways