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The development of clinical activity in relapsing-remitting MS is associated with a decrease of FasL mRNA and an increase of Fas mRNA in peripheral blood

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Author: Lopatinskaya, L. · Boxel van-Dezaire, A.H.H. · Barkhof, F. · Polman, C.H. · Lucas, C.J. · Nagelkerken, L.
Type:article
Date:2003
Source:Journal of Neuroimmunology, 1-2, 138, 123-131
Identifier: 237074
doi: doi:/10.1016/S0165-5728(03)00089-4
Keywords: Health · CCR3 · CCR5 · CXCR3 · Fas (Apo-1, CD95) · Fas Ligand (CD95L, CD178) · Chemokine receptor CCR3 · Chemokine receptor CCR5 · Chemokine receptor CXCR3 · Fas antigen · FAS ligand · Messenger RNA · Blood · Cell migration · Central nervous system · Clinical article · Controlled study · Disease activity · Disease exacerbation · Inflammatory cell · Mononuclear cell · Multiple sclerosis · Protein expression · Adult · Antigens, CD95 · Apoptosis · Cross-Sectional Studies · Down-Regulation · Fas Ligand Protein · Humans · Ligands · Longitudinal Studies · Membrane Glycoproteins · Middle Aged · Multiple Sclerosis, Chronic Progressive · Multiple Sclerosis, Relapsing-Remitting · Receptors, CCR5 · Receptors, Chemokine · RNA, Messenger · Up-Regulation

Abstract

In this longitudinal study, we examined the expression of Fas, FasL, CCR3, CCR5 and CXCR3 mRNA in peripheral blood mononuclear cells (PBMCs) of secondary progressive (SP) and relapsing-remitting (RR) multiple sclerosis (MS) patients. In RR patients, FasL, CCR3 and CCR5 mRNA levels were increased prior to the exacerbations, but these decreased during clinical activity, while mRNA levels of Fas increased. SP patients have increased the levels of Fas and FasL mRNA; the latter was particularly increased during lesional activity. Our data support the hypothesis that changes in Fas and FasL mRNA related to clinical activity are due to the migration of inflammatory cells to the central nervous system (CNS). © 2003 Elsevier Science B.V. All rights reserved. Chemicals/CAS: Antigens, CD95; CC chemokine receptor 3; CXC chemokine receptor 3; Fas Ligand Protein; FASLG protein, human; Ligands; Membrane Glycoproteins; Receptors, CCR5; Receptors, Chemokine; RNA, Messenger