TNFRSF18 and Alzheimer disease: This may partly account for the significant attenuation of the inflammatory molecules in the brain obtained by neutralization of TNFSF10, which also recruits Treg cells [16], Interestingly, we showed that the human post-mortem AD brain expressed CD3 (which was not expressed by the healthy human brain), that co-localized with FoxP3 and GITR, corroborating the hypothesis that the AD brain is also characterized by the presence of immunocytes, in analogy with other immune-related CNS disorders [49].