Chronic inflammation is usually associated with accumulation of non-degradable substances, viral infection, and autoimmune disorders. In these situations, prolonged activation of immune cells can lead to tissue destruction, fibrosis, and uncontrolled angiogenesis. Despite the eyes are immune-privileged sites, deposition of inflammatory proteins in the drusen and observation of multiple types of immune cells in AMD eyes[9] indicate that this privilege is likely revoked. The immune-privileged of retina is achieved by formation of vascular barrier and secretion of immunosuppressive molecules[10]. RPE cells can modulate retinal immune response by secretion of immunosuppressive molecules PGE2 and PEDF to suppress T cell and macrophage activation, respectively [11, 12]. In addition, challenging RPE cells with excessive amount of preoxidized photoreceptor outer segments (Ox-POS) can induce expression of IL-8 and MCP-1 to recruit and activate immune cells[13].
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Infiltration of macrophages is commonly observed in both forms of advanced AMD. Activated macrophages can induce death of RPE by activation of the complement cascade or induce apoptosis by a contact dependent mechanism [14, 15]. Based on functions, cytokine profiles, and surface markers, macrophages can be classified as M1 (pro-inflammatory) and M2 macrophages (pro-angiogenic). These two types of macrophages carry out distinct biological functions but they are interchangeable upon stimulations. M1 macrophages promote inflammatory response by secretion of cytokines such as IL-1β, IL-6, and TNF-α. M2 macrophages are involved in scavenging, tissue repair, and angiogenesis. Recently, a pilot study had revealed a preferential increase of M1 population in GA and M2 population in CNV[16]. However, whether this change in macrophage subtypes is an initiative or a consequence of different forms of AMD need to be further
Infiltration of macrophages is commonly observed in both forms of advanced AMD. Activated macrophages can induce death of RPE by activation of the complement cascade or induce apoptosis by a contact dependent mechanism [14, 15]. Based on functions, cytokine profiles, and surface markers, macrophages can be classified as M1 (pro-inflammatory) and M2 macrophages (pro-angiogenic). These two types of macrophages carry out distinct biological functions but they are interchangeable upon stimulations. M1 macrophages promote inflammatory response by secretion of cytokines such as IL-1β, IL-6, and TNF-α. M2 macrophages are involved in scavenging, tissue repair, and angiogenesis. Recently, a pilot study had revealed a preferential increase of M1 population in GA and M2 population in CNV[16]. However, whether this change in macrophage subtypes is an initiative or a consequence of different forms of AMD need to be further