Targeting T cells responsive to the priming epitope prevent the relapsing phase of experimental autoimmune encephalomyelitis

• Relapsing EAE develops following recovery from primary disease
• Prevention of the relapse phase occurs with peptide specific reagents
• Peptide reagents targeting the primary disease inducing epitope prevent relapse
• Pathogenic epitope spread does not appear to play a role in this model of EAE

Upon recovery from the initial episode of experimental autoimmune encephalomyelitis (EAE), virtually all SJL mice develop relapsing/remitting episodes of disease. These relapses may occur due to the reactivation of memory T cells initially stimulated as part of the disease-inducing protocol or naïve T-cell populations stimulated by distinct encephalitogens derived from the inflammatory disease process (epitope spread). We have used encephalitogen-specific non-linear peptide octamers to modify the course of relapsing EAE (rEAE) in SJL mice immunized with an oliogodendrocyte-specific protein peptide (OSP 55–71). Our studies show that the peptide-octamers, which target the T cells stimulated by the priming encephalitogen, but not other candidate encephalitogens, prevent rEAE.