ausblenden:
Schlagwörter:
AUTOIMMUNE INFLAMMATION; DIFFERENTIAL REGULATION; BETA THERAPY; CELLS;
IL-16; ACTIVATION; ENCEPHALOMYELITIS; EXPRESSION; MONOCYTES; CYTOKINEexperimental autoimmune encephalomyelitis; interferon-; interleukin-16;
multiple sclerosis; Th17 cells; treatment;
Zusammenfassung:
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.
