Interferon β‐1a reduces increased interleukin‐16 levels in multiple sclerosis patients. (25th January 2014)

• Record Type: Journal Article
• Authors: Nischwitz, S.; Faber, H.; Sämann, P. G.; Domingues, H. S.; Krishnamoorthy, G.; Knop, M.; Müller‐Sarnowski, F.; Yassouridis, A.; Weber, F.
• Is Part Of: Acta neurologica Scandinavica. Volume 130:Number 1(2014:Jul.)
• Page Start: 46
• Page End: 52
• Publication Date: 2014-01-25
• Subjects: Neurology -- Periodicals; 616.8
• DOI: 10.1111/ane.12215
• Languages: English
• ISSNs: 0001-6314

Abstract

<abstract abstract-type="main" id="ane12215-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="ane12215-sec-0001" sec-type="section"> <title>Objectives</title> <p>There is convergent evidence for an important role of interleukin‐16 (IL‐16) in the pathogenesis of multiple sclerosis (MS). IL‐16 serves as a chemoattractant for different immune cells that are involved in developing lesions. Here, we compared IL‐16 levels of MS patients and controls and addressed the long‐term effect of IFN‐<italic>β</italic>, the most common immunomodulatory MS therapy, on IL‐16 serum levels in MS patients over 2 years. Beyond this, we analysed the expression of IL‐16 in two CD4<sup>+</sup> T‐cell subsets, Th1 and Th17 cells, which are important autoimmune mediators and affected by IFN‐<italic>β</italic> treatment, derived from myelin‐specific T‐cell transgenic mice.</p> </sec> <sec id="ane12215-sec-0002" sec-type="section"> <title>Materials and methods</title> <p>IL‐16 serum levels of 17 controls and of 16 MS patients before therapy and at months 1, 2, 3, 6, 9, 12 and 24 during IFN‐<italic>β</italic>1a therapy were determined by ELISA. MRI was performed before therapy, at months 12 and 24. IL‐16 expression of <italic>in vitro</italic> differentiated murine myelin oligodendrocyte glycoprotein (MOG)‐specific Th1 and Th17 cells was quantified by real‐time PCR.</p> </sec> <sec id="ane12215-sec-0003" sec-type="section"> <title>Results</title> <p>Before therapy, MS patients showed significantly elevated IL‐16 levels compared with controls irrespective of disease activity determined by MRI. Therapy with IFN‐<italic>β</italic>1a led to a significant linear decrease in IL‐16 serum levels beginning after 2 months. MOG‐specific Th17 cells expressed more IL‐16 than Th1 cells.</p> </sec> <sec id="ane12215-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Reduction in increased IL‐16 levels may be of relevance for the therapeutic effect of IFN‐<italic>β</italic>1a in MS. Easily accessible IL‐16 serum levels hold a potential as biomarker of treatment efficacy in MS.</p> </sec> </abstract>