The expression of CD59 in experimental allergic neuritis

Complement is implicated as an effector in inflammatory demyelination occur ring in Guillain-Barre syndrome (CBS) and in experimental allergic neuritis (EAN). CD59, a potent complement regulatory protein that inhibits the form ation of the terminal cytolytic membrane attack complex (MAC), is expressed on human and rat Schwann cells. In EAN the expression of CD59 was increase d on Schwann cells during demyelination and axonal degeneration, evaluated by immunostaining of nerve sections and teased fibres. Mac-1 (CD1 Ib) posit ive leukocytes were localized close to the Schwann cells showing enhanced C D59 staining. The increased CD59 expression in EAN could therefore be due t o the release of cytokines or other immunoregulatory molecules from the inf lammatory cells. However, interferon gamma (LFN-gamma) or tumor necrosis fa ctor alfa (TNF-alpha) did not upregulate the expression of CD59 on rat Schw ann cells in culture. The increased expression of CD59 in EAN is likely to be important in the protection of Schwann cells from MAC. (C) 1999 Elsevier Science B.V. All rights reserved.