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. 2019 Sep 9;9:12903. doi: 10.1038/s41598-019-49472-8

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of major mechanisms involved in immuno-metabolic modulation of retinal inflammation by CD36 ligand MPE-001. Retinal inflammation induced by photo-oxidative stress induces subretinal MP accumulation, pro-inflammatory cytokine production and photoreceptor degeneration (left panel). Treatment with MPE-001 diminishes subretinal MP accumulation, reduces pro-inflammatory cytokine production and as a result protects photoreceptors (right panel). MPE-001 exerts these benefits by dissociating the CD36-TLR2/6 complex, attenuating NF-κB and NLRP3-dependent inflammasome activation, and in addition by increasing COX-2 and PPAR-γ which also mitigates inflammation as it induces an aerobic metabolic shift in MPs (right panel).