Congruent effects of estrogen and T-cell receptor peptide therapy on regulatory T cells in EAE and MS

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19 Citations (Scopus)

Abstract

Both estrogen (E2) and T-cell receptor (TCR) peptides have beneficial effects on the clinical course of experimental autoimmune encephalomyelitis (EAE) and possibly multiple sclerosis (MS) that involve distinct but congruent mechanisms. Of interest, these two approaches share an ability to enhance expression of the FoxP3 gene and associated activity of regulatory T (Treg) cells. E2 increases the number and activity of FoxP3+ T cells through Esr-1 signaling during TCR activation of CD4+CD25- T cells. In contrast, TCR peptide therapy appears to increase the frequency of regulatory FoxP3+ T cells specific for self-TCR determinants expressed by targeted pathogenic T cells. The combined effects on Treg expansion and activation induced by these distinct immunoregulatory approaches may account for their potent effects on clinical EAE and argue for a similar combined therapeutic approach for MS.

Original languageEnglish (US)
Pages (from-to)447-477
Number of pages31
JournalInternational Reviews of Immunology
Volume24
Issue number5-6
DOIs
StatePublished - Sep 2005

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Autoimmune Experimental Encephalomyelitis
Regulatory T-Lymphocytes
T-Cell Antigen Receptor
Multiple Sclerosis
Estrogens
Peptides
T-Lymphocytes
Therapeutics
Gene Expression

Keywords

  • Estrogen
  • Experimental autoimmune encephalomyelitis
  • FoxP3
  • Multiple sclerosis
  • T cell receptor
  • Therapy

ASJC Scopus subject areas

  • Immunology

Cite this

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abstract = "Both estrogen (E2) and T-cell receptor (TCR) peptides have beneficial effects on the clinical course of experimental autoimmune encephalomyelitis (EAE) and possibly multiple sclerosis (MS) that involve distinct but congruent mechanisms. Of interest, these two approaches share an ability to enhance expression of the FoxP3 gene and associated activity of regulatory T (Treg) cells. E2 increases the number and activity of FoxP3+ T cells through Esr-1 signaling during TCR activation of CD4+CD25- T cells. In contrast, TCR peptide therapy appears to increase the frequency of regulatory FoxP3+ T cells specific for self-TCR determinants expressed by targeted pathogenic T cells. The combined effects on Treg expansion and activation induced by these distinct immunoregulatory approaches may account for their potent effects on clinical EAE and argue for a similar combined therapeutic approach for MS.",
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