There is an accumulating body of evidence that immunological mechanisms play a prominent role in the pathogenesis of diabetic retinopathy (DR), which is characterized by many features typical of inflammation. The upregulation of cytokines and other inflammatory mediators leading to persistent low-grade inflammation and an influx of leukocytes, is believed to contribute actively to DR-associated damage to the retinal vasculature and retinal neovascularization. This review will describe preclinical and clinical studies that document an inflammatory basis for DR and that support the use of nonsteroidal anti-inflammatory drugs, corticosteroids, and anti-vascular endothelial growth factor agents in its treatment. In addition, emerging therapeutic approaches based on ongoing investigations will be discussed, including those involving blockade of angiotensin receptors and other molecular targets such as tumor necrosis factor-α.