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. 2019 Jan 19;20(2):426. doi: 10.3390/ijms20020426

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic representation of the available literature data indicating the role of PPARs and PGC-1α in EAE. EAE: experimental autoimmune encephalomyelitis, IL-6: interleukin-6, PPAR: peroxisome proliferator-activated receptor, Sirt1: Sirtuin (silent mating type information regulation 2 homolog) 1, SRC: steroid receptor coactivator, Th: T helper lymphocyte. Large bold arrows point towards the phenotype resulted by the pharmacological or genetic interventions (gray up arrows point to amelioration of EAE, black down arrows point to exacerbation of EAE or relevant similar pathology). Small up and down arrows represent increase and decrease in number, respectively. Tilde (~) used after a term represent ‘insufficient or contrasting evidence’, whereas it represents ‘resemblance’ when used before a term.