This prediction is supported by studies on the CD200-CD200 receptor interaction, a cell-cell communication system closely related to that of CD172a and CD47 (Barclay et al., 2002), which maintains microglia in a quiescent state and has been shown to be instrumental in reducing increases in microglial numbers and activation in mouse models of autoimmune and toxoplasma-induced encephalitis (Hoek et al., 2000; Deckert et al., 2006). The gene discussed is CD200; the disease is encephalitis.