Age related macular degeneration (AMD) is a complex multifactorial disease caused by the interplay of age and genetic and environmental risk factors. A common feature observed in early and both forms of late AMD is the breakdown of the physiologically immunosuppressive subretinal environment and the protracted accumulation of mononuclear phagocytes (MP). We here discuss the origin and nature of subretinal MPs, the mechanisms that lead to their accumulation, the inflammatory mediators they produce as well as the consequences of their chronic presence on photoreceptors, retinal pigment epithelium and choroid. Recent advances highlight how both genetic and environmental risk factors directly promote subretinal inflammation and tip the balance from a beneficial inflammation that helps control debris accumulation to detrimental chronic inflammation and destructive late AMD. Finally, we discuss how changes in life style or pharmacological intervention can help to break the vicious cycle of inflammation and degeneration, restore the immunosuppressive properties of the subretinal space, and reestablish homeostasis.

年龄相关性黄斑变性（AMD）是一种复杂的多因素疾病，由年龄，遗传和环境风险因素的相互作用引起。在早期和晚期两种形式的AMD中观察到的共同特征是生理免疫抑制性视网膜下环境的破坏和单核吞噬细胞（MP）的长期积累。我们在这里讨论视网膜下MP的起源和性质，导致其积聚的机制，它们产生的炎症介质以及它们长期存在对感光器，视网膜色素上皮和脉络膜的后果。最近的进展突显了遗传和环境风险因素如何直接促进视网膜下炎症，并从有益的炎症平衡平衡，有益的炎症有助于控制碎片的积累，从而不利于慢性炎症和破坏性晚期AMD。最后，我们讨论了生活方式或药理学干预的变化如何帮助打破炎症和变性的恶性循环，恢复视网膜下间隙的免疫抑制特性并重新建立体内平衡。