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Journal Article

Interferon-1a reduces increased interleukin-16 levels in multiple sclerosis patients

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons80459

Nischwitz,  S.
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80321

Faber,  H.
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80505

Saemann,  P. G.
Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80403

Knop,  M.
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80452

Müller-Sarnowski,  F.
Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80601

Yassouridis,  A.
Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80578

Weber,  F.
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Nischwitz, S., Faber, H., Saemann, P. G., Domingues, H. S., Krishnamoorthy, G., Knop, M., et al. (2014). Interferon-1a reduces increased interleukin-16 levels in multiple sclerosis patients. ACTA NEUROLOGICA SCANDINAVICA, 130(1), 46-52. doi:10.1111/ane.12215.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0024-ACC8-D
Abstract
Objectives 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-, the most common immunomodulatory MS therapy, on IL-16 serum levels in MS patients over 2years. Beyond this, we analysed the expression of IL-16 in two CD4+ T-cell subsets, Th1 and Th17 cells, which are important autoimmune mediators and affected by IFN- treatment, derived from myelin-specific T-cell transgenic mice. Materials and methods 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-1a therapy were determined by ELISA. MRI was performed before therapy, at months 12 and 24. IL-16 expression of in vitro differentiated murine myelin oligodendrocyte glycoprotein (MOG)-specific Th1 and Th17 cells was quantified by real-time PCR. Results Before therapy, MS patients showed significantly elevated IL-16 levels compared with controls irrespective of disease activity determined by MRI. Therapy with IFN-1a led to a significant linear decrease in IL-16 serum levels beginning after 2months. MOG-specific Th17 cells expressed more IL-16 than Th1 cells. Conclusions Reduction in increased IL-16 levels may be of relevance for the therapeutic effect of IFN-1a in MS. Easily accessible IL-16 serum levels hold a potential as biomarker of treatment efficacy in MS.