Aging-US: Retinal Pigment Epithelial Cells – Implication in Subretinal Immune Privilege

Aging-US published a Special Collection on Eye Disease which included "The expression of C1 inhibitor (C1INH) in macrophages is upregulated by retinal pigment epithelial cells – implication in subretinal immune privilege in the aging eye" which reported that this study aimed to understand how complement expression in macrophages is regulated by retinal pigment epithelium (RPE) RPE can modulate macrophage complement expression at the retina-choroidal interface even under aging or oxidative conditions. During inflammation, they may promote the alternative pathway of complement activation through down-regulating CFH and CD59a and upregulating C3, CFB and C1INH. When BMDMs were treated with apoptotic RPE, the expression of C1qb, CFH, and CD 59a was reduced but increased in BMDM. TNF-α pre-treated RPE enhanced C1inH and CFB expression. Dr. Heping Xu from The Queen’s University Belfast as well as The Central South University said, "The neuronal retina is segregated from the systemic immune system by the blood retina barriers (BRB) and is considered as an immune privileged tissue." The immune suppressive microenvironment of the eye is critical for retinal immune privilege. Despite the lack of systemic immune surveillance, the retina is well-protected by its own innate immune defence system, including innate immune cells and the complement system. During aging, the expression of complement proteins or fragments is increased in the retina, particularly at the retina-choroid interface. Subretinal macrophages in the healthy adult eyes (6 -12 months old) often have a small soma and long- fine-dendrites (Fig. 1A), whereas the cells in the aging eye (20 – 27 months) have a large cell body that often contains pigmented debris. This suggests that they are active phagocytizing debris released by stressed RPE cells. The Xu Research Team concluded in their Aging-US Research Output, "we show that RPE cells can modulate macrophage complement expression. Under normal aging conditions, RPE cells may convert macrophages into a phenotype that can suppress complement activation with enhanced phagocytosis. This immune regulatory function of RPE cells on macrophages may be lost under inflammatory conditions. Instead, inflammatory or apoptotic RPE cells promote macrophages to produce complement components necessary for the AP activation. RPE cells together with subretinal macrophages critically control complement activation at the retina-choroid interface in the ageing eye." Full Text - https://www.aging-us.com/article/101474/text Correspondence to: Heping Xu email: heping.xu@qub.ac.uk Keywords: macrophages, retinal pigment epithelial cells, complement, aging, subretinal immune privilege About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM