title: Cytokines and adhesion molecules in multiple sclerosis patients treated with interferon-beta1b.
abstract: Multiple sclerosis (MS), an inflammatory, demyelinating disease of the central nervous system (CNS), is thought to be caused by a T cell-mediated attack on CNS myelin and axons. Recombinant interferon (IFN)-beta is an established treatment of multiple sclerosis, and is known to reduce the number of disease relapses and the development of irreversible symptoms and signs of disease. The mechanism of action of IFN-beta treatment is, however, not completely understood. Previous studies have suggested major effects on mononuclear cell cytokine production and T cell migration, but results have been inconsistent. We found decreases in CD4 and CD8 T cell expression of the CD49d/VLA-4 molecule, increases in plasma concentrations of soluble vascular cell adhesion molecule (sVCAM-1), and increases in plasma concentrations of tumor necrosis factor and interleukin (IL)-12 p40 chain in patients with MS who were initiated on de novo treatment with IFN-beta1b. We found only minor associations between the different changes induced by IFN-beta1b-treatment. Our findings are consistent with changes in T cell expression of CD49d/VLA-4 and induction of sVCAM-1 as important effects of treatment with IFN-beta1b in multiple sclerosis, whereas the role of changes in TNF and IL-12 p40 chain concentrations is more difficult to interpret.
authors.affiliation: The MS Clinic, Department of Neurology, University of Copenhagen, Glostrup Hospital, DK-2600 Glostrup, Denmark.
authors.forename: Jakob
authors.initials: J
authors.lastname: Jensen
authors.forename: Martin
authors.initials: M
authors.lastname: Krakauer
authors.forename: Finn
authors.initials: F
authors.lastname: Sellebjerg
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002448:Cell Adhesion; D016207:Cytokines / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D006801:Humans; D039423:Integrin alpha1 / Q000096:biosynthesis; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000627:therapeutic use*; D018664:Interleukin-12 / Q000378:metabolism; D053762:Interleukin-12 Subunit p40; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000378:metabolism*; D021122:Protein Subunits / Q000378:metabolism; D011994:Recombinant Proteins / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood / Q000378:metabolism
chemical_list: D016207:Cytokines; D039423:Integrin alpha1; D053762:Interleukin-12 Subunit p40; D021122:Protein Subunits; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000068576:Interferon beta-1b; D018664:Interleukin-12; D016899:Interferon-beta