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{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7572937","sourcedb":"PMC","sourceid":"7572937","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7572937","text":"FPRs are expressed on various cell types in the ocular region, such as corneal endothelial cells, corneal epithelial cells, conjunctival goblet cells, retinal microglia, retinal pigment cells, and lens epithelial cells94–99. Additionally, various FPR-related ocular pathologies exist, such as retinal degeneration, uveitis, polypoidal choroidal vasculopathy, corneal neovascularization, and ocular allergy97,100–103. However, here, we only discuss the role of FPRs in the cornea and conjunctiva as ocular mucosal surfaces. The cornea is located at the anterior aspect of the eye and passes light to the lens. The immune response in the cornea is unreactive compared to that in the conjunctiva, because inflammation of the cornea can affect its transparency104. FPR2 is expressed on the corneal endothelium and epithelium, and the functional activity of FPR2 in those regions has been indirectly confirmed by effects of the FPR2 antagonist WRW494,95. The cornea is a transplantable tissue, and there are several reports that the ligands of FPR2, including LXA4 and RvD1, can be beneficial during corneal transplantation. LXA4 promotes the proliferation of human corneal endothelial cells, and when added to Optisol-GS, which is the pretransplant storage fluid for corneas, LXA4 reduces corneal endothelial cell damage94. RvD1 reduces allograft mortality during corneal transplantation by regulating DC-mediated inflammatory responses105. Although RvD1 promotes corneal wound healing, it is not clear whether FPR2 mediates the effect of RvD1 in 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