title: Interferon β-1a reduces increased interleukin-16 levels in multiple sclerosis patients.
abstract: OBJECTIVE
  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-β, 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(+) T-cell subsets, Th1 and Th17 cells, which are important autoimmune mediators and affected by IFN-β treatment, derived from myelin-specific T-cell transgenic mice.
  
  
  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-β1a 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-β1a 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.
  
  
  CONCLUSIONS
  Reduction in increased IL-16 levels may be of relevance for the therapeutic effect of IFN-β1a in MS. Easily accessible IL-16 serum levels hold a potential as biomarker of treatment efficacy in MS.
authors.affiliation: RG Inflammatory Disorders of the CNS, Neurology, Max Planck Institute of Psychiatry, Munich, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Nischwitz
authors.forename: H
authors.initials: H
authors.lastname: Faber
authors.forename: P G
authors.initials: PG
authors.lastname: Sämann
authors.forename: H S
authors.initials: HS
authors.lastname: Domingues
authors.forename: G
authors.initials: G
authors.lastname: Krishnamoorthy
authors.forename: M
authors.initials: M
authors.lastname: Knop
authors.forename: F
authors.initials: F
authors.lastname: Müller-Sarnowski
authors.forename: A
authors.initials: A
authors.lastname: Yassouridis
authors.forename: F
authors.initials: F
authors.lastname: Weber
mesh_terms: D000328:Adult; D000818:Animals; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D000068556:Interferon beta-1a; D016899:Interferon-beta / Q000627:therapeutic use*; D019410:Interleukin-16 / Q000096:biosynthesis / Q000097:blood* / Q000276:immunology; D008279:Magnetic Resonance Imaging; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008875:Middle Aged; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000097:blood / Q000188:drug therapy* / Q000276:immunology*; D060888:Real-Time Polymerase Chain Reaction; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
chemical_list: D007155:Immunologic Factors; D019410:Interleukin-16; D016899:Interferon-beta; D000068556:Interferon beta-1a
keywords: Th17 cells; experimental autoimmune encephalomyelitis; interferon-β; interleukin-16; multiple sclerosis; treatment