TY - JOUR
T1 - Analysis of Vβ8.2 CDR3 sequences from spinal cord T cells of Lewis rats vaccinated or treated with TCR Vβ8.2-39-59 peptide
AU - Buenafe, Abigail C.
AU - Vainiene, Margarita
AU - Celnik, Bozena
AU - Vandenbark, Arthur A.
AU - Offner, Halina
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1995
Y1 - 1995
N2 - 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.
AB - 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.
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M3 - Article
C2 - 7636217
AN - SCOPUS:0028984576
SN - 0022-1767
VL - 155
SP - 1556
EP - 1564
JO - Journal of Immunology
JF - Journal of Immunology
IS - 3
ER -