Armati P J, Pollard J D
School of Biological Sciences Zoology, University of Sydney, NSW, Australia.
Baillieres Clin Neurol. 1996 Mar;5(1):47-64.
The Schwann cell or its myelin membrane appears to be the focus of autoimmune attack in several peripheral neuropathies. Potential Schwann cell antigens have therefore been extensively studied. Of the known Schwann cell proteins, MBP, P2, MAG, PLP, PO, PMP-22 and Connexin 32, gene defects of the latter three have recently been shown to be responsible for some forms of hereditary sensory and motor neuropathies. The L2/HNK-1 epitope, common to MAG, Po and PMP-22, is the target of autoantibody damage in neuropathies associated with certain IgM paraproteinaemias. P2, the inciting antigen in rat EAN, has no demonstrated role in human neuropathies. The same appears true for the glycolipid galactocerebroside, a neuritogen in rabbits. Gangliosides are currently under intense study, but the antigen for the common inflammatory neuropathies remains undefined. Evidence for the potential role of Schwann cells in immune modulation is provided; Schwann cells produced MHC molecules, the adhesion molecules I-CAM1, L1, L2-HNK-1, Ng-CAM, N-cadherisn, the cytokines IL-1, IL-6 and TNF-alpha and the inflammatory prostanoids, PGE-2 AND TxA2.
