Multiple sites in the body express varying degrees of immune privilege including the anterior chamber of the eye, brain, hamster cheek pouch, hair follicle, and pregnant uterus. The earliest explanation for the immune privilege of the brain suggested that the absence of conventional lymphatic vessels prevented antigens from leaving the brain and reaching regional lymph nodes, and the tight junctions between vascular endothelial cells in the brain created a blood-brain barrier that retarded extravasation of immune elements into the brain. However, subsequent studies demonstrated that the movement of macro-molecules and cells into and out of the brain was not restricted . Antigens introduced into the brain were able to leave the brain by both the venous and lymphatic routes, although the lymphatic pathway was less efficient [14, 15].
Not only do antigens introduced into the CNS escape and accumulate in cervical lymph nodes, once there, they also induce a form of immune deviation termed brain-associated immune deviation in which delayed-type hypersensi-tivity is actively suppressed in an antigen-specific manner [14, 16, 17]. Brain-associated immune deviation is believed to contribute to the immune privilege of the brain and to coincidentally reduce the risk for immune-mediated inflammation in the CNS.
In addition to the brain-associated immune deviation, the immune privilege of the brain is enhanced by the expression of cell membrane molecules that delete inflammatory cells. It is well recognized that ocular immune privilege relies on the widespread expression of Fas ligand (FasL; CD95L) on cells within the eye . Multiple cells in the CNS also express FasL; these include: astrocytes, oligodendrocytes, microglia, and the vascular endothelium . Interestingly, the microvascular endothelial cells in the CNS are believed to reduce the risk for inflammation by expressing FasL, which limits the extravasation of viable inflammatory cells [20, 21].
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