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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?

Fig. 4

PGE2–EP2 and PGE2–EP4 signalling in Th17 lymphocytes (left) and microglia/macrophages (right). PGE2 can promote the accumulation of Th17 lymphocytes in the CNS by signalling through its EP2 receptor and promotes the secretion of pro-inflammatory factors such as IFN-y and GM-CSF by signalling through its EP4 receptor. However, in monocyte-derived macrophages and microglia EP2 signalling leads to their polarization towards a pro-inflammatory phenotype, while, in contrast, EP4 signalling in these cells results in the suppression of this pro-inflammatory phenotype

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