CD200 and experimental autoimmune encephalomyelitis: As an inhibitory signal pathway, a lack of CD200 or CD200R1, which is the receptor with the highest binding affinity to CD200, resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE), increased susceptibility to collagen-induced arthritis (CIA) and aggravation of experimental autoimmune uveoretinitis (EAU) in mouse models12, 13.