Elevated CD40 Ligand Expressing Blood T‐Cell Levels in Multiple Sclerosis Are Reversed by Interferon‐Beta Treatment

Myelin protein reactive CD4+ T cells are considered to be involved in the proposed immunopathogenesis of multiple sclerosis (MS). One particularly important molecule for T‐cell activation is the CD40L (gp39) that is expressed on the surface of T cells. This study focuses on the CD40 and the CD40L ex...

Full description

Saved in:
Bibliographic Details
Published inScandinavian journal of immunology Vol. 51; no. 3; pp. 312 - 320
Main Authors Teleshova, N, Bao, W, Kivisäkk, P, Ozenci, V, Mustafa, M, Link, H
Format Journal Article
LanguageEnglish
Published Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 01.03.2000
Wiley Subscription Services, Inc
Subjects
Online AccessGet full text
ISSN0300-9475
1365-3083
DOI10.1046/j.1365-3083.2000.00688.x

Cover

More Information
Summary:Myelin protein reactive CD4+ T cells are considered to be involved in the proposed immunopathogenesis of multiple sclerosis (MS). One particularly important molecule for T‐cell activation is the CD40L (gp39) that is expressed on the surface of T cells. This study focuses on the CD40 and the CD40L expression on mononuclear cells prepared from blood from patients with MS, other neurological diseases (OND) and healthy subjects. Immunostaining followed by a three channel flow cytometry was adopted. Patients with MS had higher levels of CD3+CD40L+, CD4+CD40L+ and CD8+CD40L+ T cells compared to patients with OND and healthy subjects. Cross‐sectional comparisons revealed that the elevation of CD40L+ T cell subtypes was confined to the patients with untreated MS and not observed in the patients with MS treated with interferon‐β (IFN‐β). Follow up studies showed that levels of CD3+CD40L+ and CD4+CD40L+ T cells decreased in individual patients after the initiation of the IFN‐β treatment. The enhanced expression of CD40L on CD3+, CD4+ and CD8+ T cells in patients with MS may implicate a role for this molecule in disease immunopathogenesis.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
content type line 14
ObjectType-Article-2
ObjectType-Feature-1
content type line 23
ISSN:0300-9475
1365-3083
DOI:10.1046/j.1365-3083.2000.00688.x