Experimental autoimmune encephalomyelitis (EAE) in the Lewis rat can be induced with the administration of Gp-BP. This disease appears to be mediated at least in part by Vβ8.2+ CD4+ T cells, which specifically recognize the BP72-89 encephalitogenic peptide. Treatment or protection with Vβ8.2 CDR2 39-59 peptide can suppress or prevent clinical signs of EAE, presumably through the activation of regulatory T cells. Interestingly, Vβ8.2+ T cells continue to persist in the spinal cord of protected animals, although their appearance in the central nervous system (CNS) is delayed when compared with control animals with EAE. As part of our effort to elucidate the mechanism(s) of peptide protection and therapy, we sought to determine whether the Vβ8.2+ T cells in the spinal cord of protected or treated rats were truly representative of those found in rats with clinical EAE. Therefore, we examined the following CNS samples for the Asp96Ser97 motif, which has been identified previously in Vβ8.2+ BP-specific, encephalitogenic T cell clones: 1) rats protected with Vβ8.2-39-59 peptide, 2) rats treated with Vβ8.2-39-59 peptide, and 3) control rats with EAE. Our findings indicate that EAE-associated Vβ8.2+ sequences can still be found in both peptide- treated and peptide-protected rats. It appears that administration of Vβ8.2 CDR2 peptide does not prevent EAE-associated Vβ8.2+ T cells from infiltrating the CNS and that other mechanisms are at work to prevent the development of EAE.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1995|
ASJC Scopus subject areas
- Immunology and Allergy