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Multiple Sclerosis
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Article

Gene expression analysis of interferon-{beta} treatment in multiple sclerosis

F Sellebjerg1, P Datta2, J Larsen3, K Rieneck4, I Alsing3, A Oturai5, A Svejgaard3, P Soelberg Sørensen5, and L. P. Ryder3

1 Department of Neurology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark;
2 Department of Neurology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark; Department of Neurology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
3 Tissue Typing Laboratory, Department of Clinical Immunology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
4 Institute of Inflammation Research, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark
5 Department of Neurology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark

* To whom correspondence should be addressed.


   Abstract

Treatment with interferon-{beta} (IFN-{beta}) induces the expression of hundreds of genes in blood mononuclear cells, and the expression of several genes has been proposed as a marker of the effect of treatment with IFN-{beta}. However, to date no molecules have been identified that are stably induced by treatment with IFN-{beta}. We use DNA microarrays to study gene expression in 10 multiple sclerosis (MS) patients who began de novo treatment with IFN-{beta}. After the first injection of IFN-{beta}, the expression of 74 out of 3428 genes changed at least two-fold and statistically significantly (after Bonferroni correction). In contrast, we observed no persisting effects of IFN-{beta} on gene expression. Among the most strongly induced genes was MXA, which has been used in previous biomarker studies in MS. In addition, the study identified the induction of LGALS9 and TCIR1G, involved in negative regulation of T helper type I immunity and T-cell activation, as novel effects of IFN-{beta} therapy in MS.

Key Words: gene expression profiling, interferon-{beta}, microarray, multiple sclerosis

First published on April 11, 2008, doi:10.1177/1352458507085976

Multiple Sclerosis 2008;14:615.

A more recent version of this article appeared on June 1, 2008


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This article has been cited by other articles:


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NeurologyHome page
D. Hesse, F. Sellebjerg, and P. S. Sorensen
Absence of MxA induction by interferon {beta} in patients with MS reflects complete loss of bioactivity
Neurology, August 4, 2009; 73(5): 372 - 377.
[Abstract] [Full Text] [PDF]


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Therapeutic Advances in Neurological DisordersHome page
P. Soelberg Sorensen
Review: Neutralizing antibodies against interferon-beta
Therapeutic Advances in Neurological Disorders, September 1, 2008; 1(2): 125 - 141.
[Abstract] [PDF]



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