Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance

C. Deng, E. Goluszko, P. Christadoss

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, α146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for α146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after tolerance induction. A high dose of α146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of α146-162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered α146-162 peptide tolerized T cell proliferation, IFN-γ, and IL-10 production. The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR α146-162 peptide-induced tolerance on CD4 cells.

Original languageEnglish (US)
Pages (from-to)3458-3467
Number of pages10
JournalJournal of Immunology
Volume166
Issue number5
StatePublished - Mar 1 2001

Fingerprint

Clonal Anergy
Fas Ligand Protein
T-Lymphocyte Epitopes
Cholinergic Receptors
Apoptosis
Peptides
Autoimmune Experimental Myasthenia Gravis
Cell Proliferation
Peptide T
T-Lymphocytes
Myasthenia Gravis
Interleukin-10
Interleukin-2
Lymphocytes

ASJC Scopus subject areas

  • Immunology

Cite this

Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance. / Deng, C.; Goluszko, E.; Christadoss, P.

In: Journal of Immunology, Vol. 166, No. 5, 01.03.2001, p. 3458-3467.

Research output: Contribution to journalArticle

@article{c8a7175f84aa4bd3b6cc036fd247395a,
title = "Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance",
abstract = "The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, α146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for α146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after tolerance induction. A high dose of α146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of α146-162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered α146-162 peptide tolerized T cell proliferation, IFN-γ, and IL-10 production. The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR α146-162 peptide-induced tolerance on CD4 cells.",
author = "C. Deng and E. Goluszko and P. Christadoss",
year = "2001",
month = "3",
day = "1",
language = "English (US)",
volume = "166",
pages = "3458--3467",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "5",

}

TY - JOUR

T1 - Fas/fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance

AU - Deng, C.

AU - Goluszko, E.

AU - Christadoss, P.

PY - 2001/3/1

Y1 - 2001/3/1

N2 - The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, α146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for α146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after tolerance induction. A high dose of α146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of α146-162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered α146-162 peptide tolerized T cell proliferation, IFN-γ, and IL-10 production. The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR α146-162 peptide-induced tolerance on CD4 cells.

AB - The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, α146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for α146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after tolerance induction. A high dose of α146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of α146-162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered α146-162 peptide tolerized T cell proliferation, IFN-γ, and IL-10 production. The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR α146-162 peptide-induced tolerance on CD4 cells.

UR - http://www.scopus.com/inward/record.url?scp=0035284802&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035284802&partnerID=8YFLogxK

M3 - Article

C2 - 11207304

AN - SCOPUS:0035284802

VL - 166

SP - 3458

EP - 3467

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 5

ER -