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*
Department of Neurology and the Brain Research Institute, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095;
Division of Immune Regulation, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121; and
Research Genetics, Huntsville, AL 35801
Oligodendrocyte-specific protein (OSP) is a recently isolated and
cloned, 207-aa, hydrophobic, four-transmembrane protein found in CNS
myelin. It represents 
7% of total myelin protein. The OSP cDNA
sequence has no significant homology with previously reported genes,
but the predicted protein structure suggests that OSP is a CNS
homologue of peripheral myelin protein-22. We previously reported the
presence of anti-OSP Abs in the cerebrospinal fluid of
relapsing-remitting multiple sclerosis (MS) patients, but not control
patient groups. In this study, we tested the ability of a panel of
20-mer peptides with 10-aa overlaps, representing the sequence of
murine OSP, to induce experimental autoimmune encephalomyelitis (EAE),
an animal model for MS. SJL mice challenged with murine OSP peptides
52–71, 82–101, 102–121, 142–161, 182–201, and 192–207 exhibited
clinical EAE. OSP:52–71 elicited severe relapsing-remitting EAE in
some individuals. All other encephalitogenic peptides elicited, at
most, a loss of tail tonicity from which the mice most often completely
recovered. Mononuclear cell infiltrates and focal demyelination
characteristic of EAE were evident. T cell proliferative responses were
seen with all encephalitogenic peptides except 142–161 and 182–201.
OSP peptides 72–91 and 132–151 did not cause clinical EAE, but did
elicit robust proliferative responses. B10.PL and PL/J mice challenged
with the same OSP peptide doses as SJL mice did not exhibit clinical
EAE. These results in the SJL EAE model, together with the results from
MS patient clinical samples, make OSP a promising candidate for
autoantigenic involvement in MS.
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