title: A comparison of the mechanisms of action of interferon beta and glatiramer acetate in the treatment of multiple sclerosis.
abstract: BACKGROUND
  The development of immunomodulatory agents has represented a major advance in the treatment of multiple sclerosis (MS). To date, immunomodulatory agents approved for the treatment of relapsing MS in the United States include 3 forms of recombinant interferon (IFN) beta (2 formulations of IFN beta-1a and 1 of IFN beta-1b) and synthetic glatiramer acetate (GA). Recognition of how these agents work to regulate the immune system may lead to a better understanding of disease mechanisms, as well as to development of more effective therapies or combinations of therapy.
  
  
  OBJECTIVE
  This article reviews the potential mechanisms of action of IFN beta products and GA in the context of their regulatory effects on autoimmune components that may be of importance in MS.
  
  
  METHODS
  MEDLINE and Current Contents/Clinical Medicine were searched for articles published in English from 1993 to the present using the search terms interferon beta, glatiramer acetate, and multiple sclerosis.
  
  
  RESULTS
  IFN beta products affect the disease process in MS through multiple potential mechanisms of action, including antiviral, antiproliferative, and anti-inflammatory effects. The mechanisms of action of GA are less clear, but may involve immune regulation induced by a gradual shift of T-cell phenotype from proinflammatory (type 1 T-helper cells) to anti-inflammatory (type 2 T-helper cells) and interference with antigen presentation.
  
  
  CONCLUSIONS
  Understanding the mechanisms of action of IFN beta products and GA provides important insights into the disease processes involved in MS.
authors.affiliation: Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA. jzang@bcm.tmc.edu
authors.forename: Jingwu
authors.initials: J
authors.lastname: Zhang
authors.forename: George
authors.initials: G
authors.lastname: Hutton
authors.forename: Ying
authors.initials: Y
authors.lastname: Zang
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D000068717:Glatiramer Acetate; D006801:Humans; D007370:Interferon Type I / Q000627:therapeutic use*; D007694:Killer Cells, Natural / Q000187:drug effects; D008213:Lymphocyte Activation / Q000187:drug effects; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology; D010455:Peptides / Q000627:therapeutic use*; D011948:Receptors, Antigen, T-Cell / Q000187:drug effects; D011994:Recombinant Proteins; D013601:T-Lymphocytes / Q000187:drug effects
chemical_list: D016207:Cytokines; D007370:Interferon Type I; D010455:Peptides; D011948:Receptors, Antigen, T-Cell; D011994:Recombinant Proteins; D000068717:Glatiramer Acetate