The effect of TCR Vβ8 peptide protection and therapy on T cell populations isolated from the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis

Andrew D. Weinberg, Bozena Celnik, Margarita Vainiene, Abigail C. Buenafe, Arthur Vandenbark, Halina Offner

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Vaccination or treatment of Lewis rats with TCR Vβ8 peptides can prevent or reverse the clinical signs of experimental autoimmune encephalomyelitis (EAE) which is mediated predominantly by Vβ8.2+ CD4+/CD45R lo T cells. However, rats protected or treated with Vβ8 peptides still developed histological lesions in the spinal cord (SC), even though they remained clinical well. We sought to discern phenotypic changes characteristic of these SC infiltrating lymphocytes. In particular, we focused on whether the immunoregulatory mechanism induced by TCR peptides caused a reduction of Vβ8.2+ T cells, or induced changes in CD45R lo or hi/CD4+ subpopulations that have been associated respectively with EAE induction or recovery. In the Vβ8 peptide vaccinated rats there was a dramatic decrease in the number of Vβ8.2+ T cells isolated from the SC early in disease. During the recovery phase, however, the number of Vβ8.2+ SC T cells was similar in protected and control groups; in contrast, there was a striking reduction in the number and size of CD45R hi/CD4+ T cells in the protected animals. In rats treated with Vβ8.2 peptide, no changes were observed in the number of SC Vβ8.2+ T cells or expression of Vβ8.2 message, but similar to vaccinated rats, there was a marked decrease in the number of CD45R hi/CD4+ T cells. These data suggest that vaccination with TCR peptides prevented the initial influx of encephalitogenic Vβ8.2+ T cells into the central nervous system (CNS), whereas treatment appeared to inactivate Vβ8.2+ T cells already present in the CNS. In both cases, TCR peptide-induced inhibition of the encephalitogenic T cells apparently preempted the need for CD45R hi/CD4+ T cells that may normally be necessary to resolve the disease.

Original languageEnglish (US)
Pages (from-to)161-170
Number of pages10
JournalJournal of Neuroimmunology
Volume49
Issue number1-2
DOIs
StatePublished - 1994

Fingerprint

Autoimmune Experimental Encephalomyelitis
Spinal Cord
T-Lymphocytes
Peptides
Population
Therapeutics
Vaccination
Central Nervous System
Lymphocytes

Keywords

  • CD45R
  • Experimental autoimmune encephalomyelitis
  • Spinal cord
  • TCR peptide
  • Vβ8.2

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Clinical Neurology
  • Neurology

Cite this

The effect of TCR Vβ8 peptide protection and therapy on T cell populations isolated from the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis. / Weinberg, Andrew D.; Celnik, Bozena; Vainiene, Margarita; Buenafe, Abigail C.; Vandenbark, Arthur; Offner, Halina.

In: Journal of Neuroimmunology, Vol. 49, No. 1-2, 1994, p. 161-170.

Research output: Contribution to journalArticle

@article{49a3c254a7d94350bbdc7f9b38d42b10,
title = "The effect of TCR Vβ8 peptide protection and therapy on T cell populations isolated from the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis",
abstract = "Vaccination or treatment of Lewis rats with TCR Vβ8 peptides can prevent or reverse the clinical signs of experimental autoimmune encephalomyelitis (EAE) which is mediated predominantly by Vβ8.2+ CD4+/CD45R lo T cells. However, rats protected or treated with Vβ8 peptides still developed histological lesions in the spinal cord (SC), even though they remained clinical well. We sought to discern phenotypic changes characteristic of these SC infiltrating lymphocytes. In particular, we focused on whether the immunoregulatory mechanism induced by TCR peptides caused a reduction of Vβ8.2+ T cells, or induced changes in CD45R lo or hi/CD4+ subpopulations that have been associated respectively with EAE induction or recovery. In the Vβ8 peptide vaccinated rats there was a dramatic decrease in the number of Vβ8.2+ T cells isolated from the SC early in disease. During the recovery phase, however, the number of Vβ8.2+ SC T cells was similar in protected and control groups; in contrast, there was a striking reduction in the number and size of CD45R hi/CD4+ T cells in the protected animals. In rats treated with Vβ8.2 peptide, no changes were observed in the number of SC Vβ8.2+ T cells or expression of Vβ8.2 message, but similar to vaccinated rats, there was a marked decrease in the number of CD45R hi/CD4+ T cells. These data suggest that vaccination with TCR peptides prevented the initial influx of encephalitogenic Vβ8.2+ T cells into the central nervous system (CNS), whereas treatment appeared to inactivate Vβ8.2+ T cells already present in the CNS. In both cases, TCR peptide-induced inhibition of the encephalitogenic T cells apparently preempted the need for CD45R hi/CD4+ T cells that may normally be necessary to resolve the disease.",
keywords = "CD45R, Experimental autoimmune encephalomyelitis, Spinal cord, TCR peptide, Vβ8.2",
author = "Weinberg, {Andrew D.} and Bozena Celnik and Margarita Vainiene and Buenafe, {Abigail C.} and Arthur Vandenbark and Halina Offner",
year = "1994",
doi = "10.1016/0165-5728(94)90192-9",
language = "English (US)",
volume = "49",
pages = "161--170",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - The effect of TCR Vβ8 peptide protection and therapy on T cell populations isolated from the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis

AU - Weinberg, Andrew D.

AU - Celnik, Bozena

AU - Vainiene, Margarita

AU - Buenafe, Abigail C.

AU - Vandenbark, Arthur

AU - Offner, Halina

PY - 1994

Y1 - 1994

N2 - Vaccination or treatment of Lewis rats with TCR Vβ8 peptides can prevent or reverse the clinical signs of experimental autoimmune encephalomyelitis (EAE) which is mediated predominantly by Vβ8.2+ CD4+/CD45R lo T cells. However, rats protected or treated with Vβ8 peptides still developed histological lesions in the spinal cord (SC), even though they remained clinical well. We sought to discern phenotypic changes characteristic of these SC infiltrating lymphocytes. In particular, we focused on whether the immunoregulatory mechanism induced by TCR peptides caused a reduction of Vβ8.2+ T cells, or induced changes in CD45R lo or hi/CD4+ subpopulations that have been associated respectively with EAE induction or recovery. In the Vβ8 peptide vaccinated rats there was a dramatic decrease in the number of Vβ8.2+ T cells isolated from the SC early in disease. During the recovery phase, however, the number of Vβ8.2+ SC T cells was similar in protected and control groups; in contrast, there was a striking reduction in the number and size of CD45R hi/CD4+ T cells in the protected animals. In rats treated with Vβ8.2 peptide, no changes were observed in the number of SC Vβ8.2+ T cells or expression of Vβ8.2 message, but similar to vaccinated rats, there was a marked decrease in the number of CD45R hi/CD4+ T cells. These data suggest that vaccination with TCR peptides prevented the initial influx of encephalitogenic Vβ8.2+ T cells into the central nervous system (CNS), whereas treatment appeared to inactivate Vβ8.2+ T cells already present in the CNS. In both cases, TCR peptide-induced inhibition of the encephalitogenic T cells apparently preempted the need for CD45R hi/CD4+ T cells that may normally be necessary to resolve the disease.

AB - Vaccination or treatment of Lewis rats with TCR Vβ8 peptides can prevent or reverse the clinical signs of experimental autoimmune encephalomyelitis (EAE) which is mediated predominantly by Vβ8.2+ CD4+/CD45R lo T cells. However, rats protected or treated with Vβ8 peptides still developed histological lesions in the spinal cord (SC), even though they remained clinical well. We sought to discern phenotypic changes characteristic of these SC infiltrating lymphocytes. In particular, we focused on whether the immunoregulatory mechanism induced by TCR peptides caused a reduction of Vβ8.2+ T cells, or induced changes in CD45R lo or hi/CD4+ subpopulations that have been associated respectively with EAE induction or recovery. In the Vβ8 peptide vaccinated rats there was a dramatic decrease in the number of Vβ8.2+ T cells isolated from the SC early in disease. During the recovery phase, however, the number of Vβ8.2+ SC T cells was similar in protected and control groups; in contrast, there was a striking reduction in the number and size of CD45R hi/CD4+ T cells in the protected animals. In rats treated with Vβ8.2 peptide, no changes were observed in the number of SC Vβ8.2+ T cells or expression of Vβ8.2 message, but similar to vaccinated rats, there was a marked decrease in the number of CD45R hi/CD4+ T cells. These data suggest that vaccination with TCR peptides prevented the initial influx of encephalitogenic Vβ8.2+ T cells into the central nervous system (CNS), whereas treatment appeared to inactivate Vβ8.2+ T cells already present in the CNS. In both cases, TCR peptide-induced inhibition of the encephalitogenic T cells apparently preempted the need for CD45R hi/CD4+ T cells that may normally be necessary to resolve the disease.

KW - CD45R

KW - Experimental autoimmune encephalomyelitis

KW - Spinal cord

KW - TCR peptide

KW - Vβ8.2

UR - http://www.scopus.com/inward/record.url?scp=0028178570&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028178570&partnerID=8YFLogxK

U2 - 10.1016/0165-5728(94)90192-9

DO - 10.1016/0165-5728(94)90192-9

M3 - Article

VL - 49

SP - 161

EP - 170

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -