PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis

<table><i>A model for PPAR-<svg height="7.1750002" id="M4" style="vertical-align:-0.1254pt" version="1.1" viewbox="0 0 8.9375 7.1750002" width="8.9375" xmlns="http://www.w3.org/2000/svg">
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</svg>-mediated protection in EAE</i>. 
In the presence of PPAR-<svg height="13.425" id="M5" style="vertical-align:-2.29482pt" version="1.1" viewbox="0 0 8.8500004 13.425" width="8.8500004" xmlns="http://www.w3.org/2000/svg">
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</svg> agonists, PPAR-<svg height="10.7375" id="M6" style="vertical-align:-0.13794pt" version="1.1" viewbox="0 0 7.9875002 10.7375" width="7.9875002" xmlns="http://www.w3.org/2000/svg">
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</svg> heterodimerizes with RXR, dissociates from its nuclear corepressor complex, associates with a coactivator complex, and binds to PPREs in the promoter region of IL-4 and/or IL-5. The transactivation of IL-4/IL-5 leads to increased expression of GATA-3 which in turn results in decreased T-bet expression and downregulation of the Th1/Th17 inflammatory response. This shift in the immune response to a Th2-like phenotype results in amelioration of EAE.
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PPAR Research

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Figure 1

Figure 1: PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis 