The expression of complement regulatory proteins by adult human oligodendrocytes

J Neuroimmunol. 1998 Apr 1;84(1):69-75. doi: 10.1016/s0165-5728(97)00241-5.


In multiple sclerosis, infiltrating T lymphocytes and perivascular microglia may initiate demyelinating lesions, but a role for antibody and complement in the ensuing inflammatory damage to myelin and oligodendrocytes is likely. In most tissues, ubiquitously expressed complement regulatory proteins prevent autologous destruction, protecting host cells from the powerful cytolytic activity of activated complement. We have studied the surface expression of a comprehensive range of complement regulatory proteins by live adult human oligodendrocytes in vitro. Only DAF of the activation pathway regulators was expressed, not CR1 or MCP. Of the membrane attack pathway regulatory proteins, HRF was not expressed, while substantial heterogeneity of CD59 expression by oligodendrocytes was found. Clusterin expression was not found. A relative deficiency of protective complement regulatory proteins on human oligodendrocytes may contribute to their selective damage in multiple sclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD59 Antigens / metabolism
  • Cells, Cultured
  • Clusterin
  • Complement Inactivator Proteins / immunology
  • Complement Inactivator Proteins / metabolism*
  • Complement Membrane Attack Complex / immunology
  • Complement Membrane Attack Complex / metabolism*
  • Complement System Proteins / immunology
  • Complement System Proteins / metabolism*
  • Demyelinating Diseases / immunology
  • Demyelinating Diseases / metabolism*
  • Glycoproteins / analysis
  • Humans
  • Molecular Chaperones*
  • Multiple Sclerosis / immunology
  • Oligodendroglia / immunology
  • Oligodendroglia / metabolism*


  • CD59 Antigens
  • CLU protein, human
  • Clusterin
  • Complement Inactivator Proteins
  • Complement Membrane Attack Complex
  • Glycoproteins
  • Molecular Chaperones
  • Complement System Proteins