Abstract
The ocular tissue microenvironment is immune privileged and uses several mechanisms of immunosuppression to prevent the induction of inflammation. Besides being a blood-barrier and source of photoreceptor nutrients, the retinal pigment epithelial cells (RPE) regulate the activity of immune cells within the retina. These mechanisms involve the expression of immunomodulating molecules that make macrophages and microglial cells suppress inflammation and promote immune tolerance. The RPE have an important role in ocular immune privilege to regulate the behavior of immune cells within the retina. Reviewed is the current understanding of how RPE mediate this regulation and the changes seen under pathological conditions.
Highlights
Together the results demonstrate the need for an intact retinal pigment epithelial cells (RPE) monolayer to maintain ocular immune privilege
associated immune deviation (ACAID) demonstrates that macrophages with the potential of becoming antigen presenting cells (APC) are influenced by the ocular microenvironment to promote Treg cell activation
These results suggest that while the use of alpha-Melanocyte Stimulating Hormone (a-MSH) in therapy to suppress inflammation is possible through its other receptors, it appears that the recovery of immune privilege is dependent on a-MSH working through melanocortin 5-receptor (MC5r)
Summary
The eye is called immune privileged from the original observations of prolonged allograft survival within the anterior chamber even following immunization to alloantigens [1] This includes immune regulation and immune tolerance to antigens and pathogens within the eye [2,3,4]. RPE Regulation of Retinal Immunobiology microenvironment that actively manipulates immune cells to promote the health of the visual axis, and to prevent the activation of inflammation These mechanisms of ocular immune privilege are for most of us highly effective in preventing inflammation, and the mediators of immune privilege have potential to be therapeutically adapted to suppress inflammation within the eye and in other tissues. Placing foreign antigen in the subretinal space (the temporary pocket that forms when the photoreceptors are detached from the RPE) induces an ACAID-like response [21] This has defined immune privilege to include the retina
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