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CUTTING EDGE |
*
Department of Neurology,
Department of Pathology and Laboratory Medicine, Division of Neuropathology, University of Pennsylvania, Philadelphia, PA 19104; and
Division of Clinical Neurology, University Hospital Queen’s Medical Centre, Nottingham, United Kingdom
Experimental autoimmune encephalomyelitis (EAE), an inflammatory
demyelinating disease of the CNS, is regarded as an experimental model
for multiple sclerosis. The complement has been implicated in the
pathogenesis of multiple sclerosis. To clarify the role of C in mouse
EAE, we immunized mice deficient in C3 (C3-/-) and their
wild-type (C3+/+) littermates with myelin oligodendrocyte
glycoprotein peptide 35–55. C3-/- mice were susceptible
to EAE as much as the C3+/+ mice were. No differences were
found for the production of IL-2, IL-4, IL-12, TNF-
, and IFN-
between C3+/+ and C3-/- mice. This finding
shows that C3, a key component in C activation, is not essential in
myelin oligodendrocyte glycoprotein peptide-induced EAE in
mice.
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