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*
Department of Neurology, and
Division of Clinical Immunology and Rheumatology, University of Alabama, Birmingham, AL 35294;
Department of Immunology, St Judes Childrens Research Hospital, Memphis, TN 38105;
Max Planck Institute for Neurobiology, Martinsried, Germany; and
¶ Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461
Encephalitogenic T cells that mediate experimental autoimmune
encephalomyelitis (EAE) are commonly assumed to be exclusively
CD4+, but formal proof is still lacking. In this study, we
report that synthetic peptides 3555 from myelin oligodendrocyte
glycoprotein (pMOG3555) consistently activate a high
proportion of CD8+ 
TCR+ T cells that are
encephalitogenic in C57BL/6 (B6) mice. The encephalitogenic potential
of CD8+ MOG-specific T cells was established by adoptive
transfer of CD8-enriched MOG-specific T cells. These cells induced a
much more severe and permanent disease than disease actively induced by
immunization with pMOG3555. CNS lesions in
pMOG3555 CD8+ T cell-induced EAE were
progressive and more destructive. The CD8+ T cells were
strongly pathogenic in syngeneic B6 and RAG-1-/- mice,
but not in isogeneic
2-microglobulin-deficient mice.
MOG-specific CD8+ T cells could be repeatedly reisolated
for up to 287 days from recipient B6 or RAG-1-/- mice in
which disease was induced adoptively with <1 x 106 T
cells sensitized to pMOG3555. It is postulated that MOG
induces a relapsing and/or progressive pattern of EAE by eliciting a T
cell response dominated by CD8+ autoreactive T cells. Such
cells appear to have an enhanced tissue-damaging effect and persist in
the animal for long periods.
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