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Autoimmune Diseases
Volume 2011 (2011), Article ID 485752, 8 pages
Research Article

Effects of IFN-B on TRAIL and Decoy Receptor Expression in Different Immune Cell Populations from MS Patients with Distinct Disease Subtypes

1Department of Pharmacology, Dalhousie University, Halifax, NS, Canada B3H 1X5
2Department of Neurology, Dalhousie University, Halifax, NS, Canada B3H 1V7
3Department of Psychiatry, Dalhousie University, Halifax, NS, Canada B3H 2E2

Received 23 August 2010; Accepted 16 November 2010

Academic Editor: David Dyment

Copyright © 2011 Andrea L. O. Hebb et al. 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.


Using quantitative RT-PCR, we compared mRNA levels for TRAIL [tumor necrosis factor (TNF)–related apoptosis-inducing ligand] and its receptors in various immune cell subsets derived from the peripheral blood of untreated normal subjects (NS) and patients with distinct subtypes of multiple sclerosis (MS): active relapsing-remitting MS (RRA), quiescent relapsing-remitting MS (RRQ), secondary-progressive MS (SPMS) or primary-progressive MS (PPMS). Consistent with a role for TRAIL in the mechanism of action of interferon-β (IFN-β), TRAIL mRNA levels were increased in monocytes from patients clinically responsive to IFN-β (RRQ) but not those unresponsive to this therapeutic (RRA). TRAIL-R3 (decoy receptor) expression was elevated in T cells from untreated RRMS patients while IFN-β therapy reversed this increase suggesting that IFN-β may promote the apoptotic elimination of autoreactive T cells by increasing the amount of TRAIL available to activate TRAIL death receptors. Serum concentrations of soluble TRAIL were increased to a similar extent by IFN-β therapy in RRQ, RRA and SPMS patients that had not generated neutralizing antibodies against this cytokine. Although our findings suggest altered TRAIL signaling may play a role in MS pathogenesis and IFN-β therapy, they do not support use of TRAIL as a surrogate marker for clinical responsiveness to this therapeutic.