Specificity, magnitude, and kinetics of MOG‐specific CD8+ T cell responses during experimental autoimmune encephalomyelitis

ML Ford, BD Evavold - European journal of immunology, 2005 - Wiley Online Library
ML Ford, BD Evavold
European journal of immunology, 2005Wiley Online Library
Experimental autoimmune encephalomyelitis (EAE) has traditionally been thought to be
almost exclusively mediated by CD4+ effector T cells. Here, we provide evidence for the
existence of mouse CD8+ T cells that are specific for an epitope of the myelin
oligodendrocyte glycoprotein (MOG). Using a panel of truncated MOG peptides, we have
identified the minimal epitope recognized by these T cells as MOG 37–46. This peptide,
while possessing relatively low affinity for H‐2Db, efficiently stimulates IFN‐γ production …
Abstract
Experimental autoimmune encephalomyelitis (EAE) has traditionally been thought to be almost exclusively mediated by CD4+ effector T cells. Here, we provide evidence for the existence of mouse CD8+ T cells that are specific for an epitope of the myelin oligodendrocyte glycoprotein (MOG). Using a panel of truncated MOG peptides, we have identified the minimal epitope recognized by these T cells as MOG 37–46. This peptide, while possessing relatively low affinity for H‐2Db, efficiently stimulates IFN‐γ production from MOG‐specific CD8+ T cell lines in vitro and induces EAE in vivo. To further characterize the magnitude and kinetics of expansion of the MOG‐specific CD8+ T cell population in vivo, we used MOG 37–50/H‐2Db MHC tetramers to visualize MOG‐specific CD8+ effectors in the peripheral lymphoid organs and central nervous system during the course of EAE induction and progression. Our results identify MOG‐specific CD8+ T cells in the central nervous system prior to and after the onset of disease, suggesting that CD8+ T cells are a possible target for therapeutic intervention during EAE.
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