CD4+CD25+FoxP3+PD1- Regulatory T cells in acute and stable relapsing-remitting multiple sclerosis and their modulation by therapy

Marina Saresella, Ivana Marventano, Renato Longhi, Francesca Lissoni, Daria Trabattoni, Laura Mendozzi, Domenico Caputo, Mario Clerici

Research output: Contribution to journalArticlepeer-review

Abstract

The intracellular expression of the programmed death receptor 1 (PD1) identifies a subset of naive Treg cells with enhanced suppressive ability; antigen stimulation results in the surface expression of PD1. Because the role of Treg impairments in multiple sclerosis (MS) is still contradictory, we analyzed naive PD1- and PD1+ Treg cells in peripheral blood and cerebrospinal fluid (CSF) of relapsing-remitting multiple sclerosis (RR-MS) patients and of healthy control subjects. Results showed that 1) CSF PD1- Treg cells were significantly augmented in MS patients; 2) PD1-Treg cells were significantly increased in the peripheral blood of patients with stable disease (SMS) compared to those with acute (AMS) disease, and in patients responding to glatiramer acetate (COPA) compared to AMS- and COPA-unresponsive patients; and 3) PD1+ Treg cells were similar in CSF and peripheral blood of all groups analyzed. PD1- Treg cells were not increased in the peripheral blood of interferon-β (IFNβ) -responsive patients, but the suppressive ability of Treg cells was significantly higher in SMS and in COPA- or IFNβ-responsive compared to AMS- and COPA-unresponsive individuals. The data herein suggest that PD1- Treg cells play a pivotal role in MS and offer a biological explanation for disease relapse and for the mechanism associated with response to COPA and IFNβ.

Original languageEnglish
Pages (from-to)3500-3508
Number of pages9
JournalFASEB Journal
Volume22
Issue number10
DOIs
Publication statusPublished - Oct 2008

Keywords

  • Copaxone
  • Glatiramer acetate
  • Immunology
  • Neurology
  • T lymphocytes

ASJC Scopus subject areas

  • Biochemistry
  • Biotechnology
  • Genetics
  • Molecular Biology
  • Medicine(all)

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