Table of Contents Author Guidelines Submit a Manuscript
Clinical and Developmental Immunology
Volume 12 (2005), Issue 3, Pages 203-209

Unique Gene Expression Patterns in Human T-cell Lines Generated from Multiple Sclerosis Patients by Stimulation with a Synthetic MOG Peptide

1Blood Center, Tel-Aviv University. -aviv, Israel
2Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
3Multiple Sclerosis Center, Tel-Aviv University, Tel-Aviv, Israel
4Functional Genomics Unit, Sheba Medical Center, Tel-Hashomer, Tel-Aviv University, Tel-Aviv, Israel
5Department of Immunology, Weizmann Institute of Science, Rehovot Tel-Aviv University, Tel-Aviv, Israel

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Multiple sclerosis (MS) is an autoimmune disease where T-cells activated against myelin antigens are involved in myelin destruction. Yet, healthy subjects also harbor T-cells responsive to myelin antigens, suggesting that MS patient-derived autoimmune T-cells might bear functional differences from T-cells derived from healthy individuals. We addressed this issue by analyzing gene expression patterns of myelin oligodendrocytic glycoprotein (MOG) responsive T-cell lines generated from MS patients and healthy subjects. We identified 150 transcripts that were differentially expressed between MS patients and healthy controls. The most informative 43 genes exhibited >1.5-fold change in expression level. Eighteen genes were up-regulated including BCL2, lifeguard, IGFBP3 and VEGF. Twenty five genes were down-regulated, including apoptotic activators like TNF and heat shock protein genes. This gene expression pattern was unique to MOG specific T-cell lines and was not expressed in T-cell lines reactive to tetanus toxin (TTX). Our results indicate that activation in MS that promotes T-cell survival and expansion, has its own state and that the unique gene expression pattern that characterize autoreactive T-cells in MS represent a constellation of factors in which the chronicity, timing and accumulation of damage make the difference between health and disease.