title: Interferon beta treatment of multiple sclerosis increases serum interleukin-7.
abstract: BACKGROUND
  Interleukin-7 (IL-7) is a non-redundant cytokine for T-cell development and survival. The IL-7 signaling pathway has been genetically and functionally associated with several autoimmune diseases including multiple sclerosis (MS).
  
  
  OBJECTIVE
  The objective of this paper is to elucidate the effect of the widely used immunomodulatory MS therapy interferon beta (IFNβ) on IL-7 homeostasis.
  
  
  METHODS
  Swedish MS patients were screened for IL-7 concentration in serum and blood cell counts. IL-7 receptor alpha chain (IL-7Rα) expression was determined by semi-quantitative real-time polymerase chain reaction (PCR) and flow cytometry.
  
  
  RESULTS
  IFNβ treatment led to significantly increased serum IL-7 levels (mean: 17 pg/ml) compared with healthy controls (mean: 7.6 pg/ml) and natalizumab-treated patients (mean: 5.3 pg/ml). In vitro and in vivo, peripheral blood leukocytes showed decreased IL-7Rα expression and IL-7 consumption upon IFNβ exposure, suggesting that their IL-7 responsiveness is impaired during treatment.
  
  
  CONCLUSIONS
  MS patients undergoing IFNβ treatment have increased serum IL-7 levels and decreased IL-7 consumption. Given IL-7's important role in T-cell immunity, this relationship may be highly relevant for IFNβ's treatment efficacy.
authors.affiliation: Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Wangko
authors.initials: W
authors.lastname: Lundström
authors.affiliation: Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Christina
authors.initials: C
authors.lastname: Hermanrud
authors.affiliation: Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Sweden.
authors.forename: Maria
authors.initials: M
authors.lastname: Sjöstrand
authors.affiliation: Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Sweden.
authors.forename: Susanna
authors.initials: S
authors.lastname: Brauner
authors.affiliation: Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Sweden.
authors.forename: Marie
authors.initials: M
authors.lastname: Wahren-Herlenius
authors.affiliation: Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Tomas
authors.initials: T
authors.lastname: Olsson
authors.affiliation: Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Virginija
authors.initials: V
authors.lastname: Karrenbauer
authors.affiliation: Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Jan
authors.initials: J
authors.lastname: Hillert
authors.affiliation: Center for Molecular Medicine, Karolinska Institutet, SE-17176 Stockholm, Sweden Anna.Fogdell-Hahn@ki.se.
authors.forename: Anna
authors.initials: A
authors.lastname: Fogdell-Hahn
mesh_terms: D057134:Antibodies, Neutralizing / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016899:Interferon-beta / Q000627:therapeutic use*; D015851:Interleukin-7 / Q000097:blood*; D009103:Multiple Sclerosis / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D060888:Real-Time Polymerase Chain Reaction; D020395:Receptors, Interleukin-7 / Q000097:blood; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology
chemical_list: D057134:Antibodies, Neutralizing; C508605:IL7 protein, human; D007166:Immunosuppressive Agents; D015851:Interleukin-7; D020395:Receptors, Interleukin-7; C415350:interleukin-7 receptor, alpha chain; D016899:Interferon-beta
keywords: Multiple sclerosis; immunology; interferon beta; natalizumab