The expression of CD59 in experimental allergic neuritis.

Complement is implicated as an effector in inflammatory demyelination occurring in Guillain-Barré syndrome (GBS) and in experimental allergic neuritis (EAN). CD59, a potent complement regulatory protein that inhibits the formation of the terminal cytolytic membrane attack complex (MAC), is expressed on human and rat Schwann cells. In EAN the expression of CD59 was increased on Schwann cells during demyelination and axonal degeneration, evaluated by immunostaining of nerve sections and teased fibres. Mac-1 (CD11b) positive leukocytes were localized close to the Schwann cells showing enhanced CD59 staining. The increased CD59 expression in EAN could therefore be due to the release of cytokines or other immunoregulatory molecules from the inflammatory cells. However, interferon gamma (IFN-gamma) or tumor necrosis factor alfa (TNF-alpha) did not upregulate the expression of CD59 on rat Schwann cells in culture. The increased expression of CD59 in EAN is likely to be important in the protection of Schwann cells from MAC.