Inflammation in Retinal Disease

Abstract

Ocular inflammation and its related complications are important causes of vision loss. Inflammatory processes have long been implicated in the pathogenesis and sequelae of noninfectious uveitis and understood to underlie the macular edema which may arise following even uncomplicated intraocular surgeries [1]. More recently, evidence has also arisen supporting a prominent role for inflammation underlying the pathogenesis of a wide array of retinal diseases, including age-related macular degeneration (AMD) [2], diabetic retinopathy (DR) [3], retinal vein occlusion (RVO) [4], and retinitis pigmentosa (RP) [5], and has suggested a role for anti-inflammatory therapies to potentially alter the severity and course of these disorders. The goal of this special issue is to highlight the latest understanding of the role of inflammation in retinal diseases, to address current questions and controversies, and to facilitate future research. Traditionally, the eye has been considered an immune privileged site. Contributing to this immune privilege is the blood-retinal barrier which consists of both an inner barrier formed by the tight junctional complexes between retinal vascular endothelial cells and an outer barrier formed by the tight junctions between the retinal pigment epithelium (RPE) cells. Research over the last 30 years has demonstrated that mechanisms beyond tissue barriers contribute to ocular immune privilege and an immunosuppressive intraocular environment. In fact, the pigment epithelial cells which line the iris, ciliary body, and retina serve an immunomodulatory role through both the secretion of soluble immunosuppressive factors as well as contact-dependent mechanisms [6]. Vision is dependent on the exquisite and precise structure of the retina, and any process which significantly disrupts retinal architecture can have a profound impact on vision. The immune response, when controlled, is an adaptive response to restore homeostasis. Alterations in retinal homeostasis secondary to aging, metabolic abnormalities, altered vascular perfusion, or degenerative genetic conditions may initiate various inflammatory cascades. In all of these settings, a prolonged, dysregulated immune response may itself be pathologic, contributing to both the pathogenesis of retinal diseases as well as vision threatening complications.