Abstract
CD200 and its receptor, CD200 receptor (CD200R), have uniaue roles in controlling damaging inflammatory processes. At present, the only identified function for CD200 is as a ligand for CD200R. These proteins interact resulting in the activation of anti-inflammatory signaling by CD200R-expressing cells. When this interaction becomes deficient with aging or disease, chronic inflammation occurs, Experimental animal studies have demonstrated the consequences of disrupting CD200-CD200R interactions in the brain, but there have been few studies in human brains. Deficiency in neuronal CD200 may explain the chronic inflammation in human neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and multiple sclerosis; however, deficits in the microglial expression of CD200R may also be of functional significance. The purpose of this review is to assess the data regarding the role of CD200-CD200R interactions in relation to the brain in order to determine if this could be a therapeutic target for human brain diseases with inflammatory components, and what additional studies are needed.