Effects of Membrane Attack Complex of Complement on Apoptosis in Experimental Autoimmune Encephalomyelitis

Ann N Y Acad Sci. 2003 Dec;1010:530-3. doi: 10.1196/annals.1299.098.

Abstract

Complement activation is involved in the initiation of inflammation and antibody-mediated demyelination in experimental autoimmune encephalomyelitis (EAE). We investigated the role of MAC in apoptosis in myelin-induced EAE in complement C5-deficient (C5-d) and C5-sufficient (C5-s) mice. The number of apoptotic cells assessed by TUNEL assay was significantly increased in C5-d mice during clinical recovery as compared with C5-s mice. Most of the apoptotic cells were lymphocytes, monocytes, and oligodendrocytes. DNA microarray was performed using total RNA extracted from spinal cords. Genes expressed higher in C5-s included members of the caspase (caspase 6, 7), TNF and TNFR families (CD27, FasL, lymphotoxin-beta R) and survivin. These results indicate that C5 and possibly MAC may be required for the limitation of inflammatory response within the central nervous system.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Complement C5 / deficiency
  • Complement Membrane Attack Complex / genetics*
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / pathology*
  • Female
  • In Situ Nick-End Labeling
  • Mice
  • Mice, Knockout
  • Oligonucleotide Array Sequence Analysis
  • RNA / genetics
  • RNA / isolation & purification
  • Spinal Cord

Substances

  • Complement C5
  • Complement Membrane Attack Complex
  • RNA