IMMUNE ATTACK ON THE SCHWANN-CELL SURFACE IN ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY

The localization, mode of action, and roles of complement in the Guill ain-Barre syndrome have been controversial. We used high-resolution im munocytochemistry to localize complement activation products in early stages of the acute inflammatory demyelinating polyneuropathy (AIDP) p attern of Guillaio-Barre syndrome. Three ATDP subjects who were autops ied had had symptoms for 3 to 9 days at the time of death. Immunocytoc hemistry was performed on etched, epoxy resin-embedded sections, and t he next thin section was compared by electron microscopy (thick/thin s ections). Many fibers had a rim of the complement activation marker C3 d and the terminal complement complex neoantigen C5b-9 along the outer surface of the Schwann cells. Ultrastructural analysis of these C3d-p ositive fibers showed mild vesicular changes of the outermost myelin l amellae. Vesicular degeneration was seen before the invasion of macrop hages into the myelin, and was the predominant change in the subject w ith symptoms for 3 days. C3d staining was not found on myelin membrane s. The results suggest that at least some forms of AIDP are complement mediated. We speculate that complement is activated by antibody bound to epitopes on the outer surface of the Schwann cell and that the res ulting complement activation initiates the vesiculation of myelin.