Ann N Y Acad Sci. 2003 Dec;1010:530-3
Niculescu T, Weerth S, Soane L, Niculescu F, Rus V, Raine CS, Shin ML, Rus H.
University of Maryland, School of Medicine, Baltimore, Maryland 21201, USA.
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.