[Effector mechanisms of PNS demyelination in Gal-C induced-EAN]

Myelin in PNS is multi-layered membranes formed by Schwann cells, and surrounds axon. Destruction of myelin sheath results in demyelination and disturbance of nerve conduction. In PNS, Charcot-Marie-Tooth disease, certain lipidoses, Guillain-Barré syndrome, lead poisoning, compression and some metabolic neuropathies can produce demyelination. In these diseases, GBS is thought to be resulted from abnormalities of immune mechanism. Recently, autoantibodies against Gal-C, P2 and GM1, and complement fixing antibodies against PNS myelin are found in some of GBS patient sera. Here, I present studies on effector mechanism of PNS demyelination using models produced by application of Galactocerebroside (Gal-C) antibodies to PNS. Mainly, three types of effector mechanisms are involved in Gal-C antibody-induced demyelination. In abundance of antibodies, complement-mediated demyelination is at work. When complements are absent, antibody dependent macrophage-mediated demyelination can be involved. Thirdly, myelin once damaged by oxidants and etc can be opsonized by antibodies and C3b, and phagocytized by macrophages. These processes may be operating in such diseases like GBS and CIDP.