The expression of CD59 in experimental allergic neuritis

Christian A. Vedeler, Giancarlo Conti, Toshiki Fujioka, Elio Scarpini, Abdolmohamad Rostami

Research output: Contribution to journalArticlepeer-review


Complement is implicated as an effector in inflammatory demyelination occurring in Guillain-Barre 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-γ) or tumor necrosis factor alfa (TNF-α) 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. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)154-159
Number of pages6
JournalJournal of the Neurological Sciences
Issue number2
Publication statusPublished - Jun 1 1999


  • CD59
  • Complement
  • Experimental allergic neuritis
  • Guillain-Barre syndrome
  • Schwann cells

ASJC Scopus subject areas

  • Ageing
  • Clinical Neurology
  • Surgery
  • Developmental Neuroscience
  • Neurology
  • Neuroscience(all)


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