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Upregulation of TRAIL expression on human T lymphocytes by interferon b and glatiramer acetate

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada

E Rastikerdar

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada

E McCrea

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada

Y Lapierre

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada

J Dörr

Institute of Neuroimmunology, Neuroscience Research Center, NWFZ 2680, Charité 10098 Berlin, Germany

A Bar-Or

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada

J P Antel

Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada, jack.antel{at}mcgill.ca

We measured the in vivo and in vitro effects of interferon (IFN)b and glatiramer acetate (GA) on the expression of the regulatory molecule, tumor necrosis factor related apoptosis inducing ligand (TRAIL), in patients with multiple sclerosis (MS). We confirmed the prior observation that TRAIL is enhanced on anti-CD3 activated T cells by the in vitro addition of IFNß. T cells from IFNß-treated patients stimulated with anti-CD3 only, had higher levels of TRAIL than untreated patients, suggesting that in vivo IFNß exposure has an effect on TRAIL expression in association with T cell activation. In vitro IFNß-induced TRAIL upregulation on anti-CD3 or phytohemagglutinin-activated T cells was comparable for IFNß-treated and non-treated MS patients and controls, indicating that IFN receptors were neither saturated nor down-regulated by current IFNß therapy. Although GAin vivo orin vitro did not induce TRAIL, the IFNß-GA combination in vitro enhanced TRAIL expression to higher levels than IFNß alone on CD4+ T cells obtained from MS patients, regardless of GA treatment status, and healthy donors, and on GA reactive T cell lines derived from GA-treated patients or controls. Whether any observed therapeutic effects of GA/IFNß combination therapy will correlate with TRAIL expression and function remains to be determined.

Key Words: flow cytometry • glatiramer acetate • interferon type I • multiple sclerosis • TRAIL • T lymphocytes

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