Whitcup Scott M, Sodhi Akrit, Atkinson John P, Holers V Michael, Sinha Debasish, Rohrer Bärbel, Dick Andrew D
Allergan, Inc., 2525 Dupont Drive, Irvine, CA 92612, USA.
Int J Inflam. 2013;2013:348092. doi: 10.1155/2013/348092. Epub 2013 May 23.
Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries; with the aging population, the negative health impacts and costs of the disease will increase dramatically over the next decade. Although the exact cause of AMD is unknown, genetic studies have implicated the complement system as well as other immune responses in disease pathogenesis and severity. Furthermore, histologic studies have shown the presence of macrophages, lymphocytes, and mast cells, as well as fibroblasts, in both atrophic lesions and with retinal neovascularization. This review summarizes discussions from the fifth annual conference of the Arnold and Mabel Beckman Initiative for Macular Research by the Inflammation and Immune Response Task Force. These deliberations focused on the role of inflammatory immune responses, including complement, inflammasomes, adaptive immune responses, and para-inflammation, unanswered questions and studies to address these questions, and potential immune-related therapeutic targets for AMD.
年龄相关性黄斑变性（AMD）是发达国家失明的主要原因；随着人口老龄化，该疾病对健康的负面影响和成本在未来十年将急剧增加。尽管AMD的确切病因尚不清楚，但基因研究表明补体系统以及其他免疫反应与疾病的发病机制和严重程度有关。此外，组织学研究显示，在萎缩性病变以及视网膜新生血管形成中均存在巨噬细胞、淋巴细胞、肥大细胞和成纤维细胞。本综述总结了阿诺德和梅布尔·贝克曼黄斑研究倡议第五届年度会议上炎症与免疫反应特别工作组的讨论内容。这些讨论聚焦于炎症免疫反应的作用，包括补体、炎性小体、适应性免疫反应和类炎症反应，未解决的问题以及针对这些问题的研究，以及AMD潜在的免疫相关治疗靶点。
