title: CD45RA+ ICAM-3+ lymphocytes in interferon-beta1b-treated and -untreated patients with relapsing-remitting multiple sclerosis.
abstract: OBJECTIVE
  Multiple sclerosis (MS) is believed to be an autoimmune disease of the human central nervous system mediated by autoreactive T cells. Interferon-beta1b (IFN-beta1b) has been shown to be effective in reducing disease activity defined by clinical and magnetic resonance imaging (MRI) criteria in relapsing-remitting MS (RRMS). Yet, the exact mechanisms by which these benefits are achieved remain unknown. CD45RA is a marker for naive T lymphocytes and intercellular adhesion molecule-3 (ICAM-3) is expressed on resting lymphocytes.
  
  
  METHODS
  Forty-eight patients with RRMS, 24 of them treated with recombinant IFN-beta1b and 24 untreated, were enrolled in this prospective study over 18 months. We investigated the percentage of CD45RA+ ICAM-3+ cells within the total lymphocyte subset in the peripheral blood serially every 3 months and in CSF once at baseline. Detailed clinical examination including Expanded Disability Status Scale (EDSS) score was performed every 3 months and cranial MRI scans were assessed every 6 months.
  
  
  RESULTS
  We found a temporary increase in the CD45RA+ ICAM-3+ lymphocyte ratio in peripheral blood of both untreated and IFN-beta1b-treated RRMS patients. Moreover, we determined a significant negative correlation (r = -0.5874; P < 0.01) between age as well as the EDSS score (r = -0.3629; P < 0.05) and the percentages of CD45RA+ ICAM-3+ lymphocytes in peripheral blood but a positive correlation between EDSS score and the CD45RA+ ICAM-3+ ratio (r = 0.3913; P < 0.05) in the CSF at baseline.
  
  
  CONCLUSIONS
  CD45RA+ ICAM-3+ lymphocyte ratio in peripheral blood might indicate immunosenescence in MS. However, from our data it cannot be finally concluded whether it is also influenced by IFN-beta1b treatment.
authors.affiliation: Research Group for Multiple Sclerosis and Neuroimmunology, Department of Neurology, Justus-Liebig University of Giessen, Giessen, Germany.
authors.forename: N
authors.initials: N
authors.lastname: Chatzimanolis
authors.forename: J
authors.initials: J
authors.lastname: Kraus
authors.forename: R
authors.initials: R
authors.lastname: Bauer
authors.forename: B
authors.initials: B
authors.lastname: Engelhardt
authors.forename: T
authors.initials: T
authors.lastname: Bregenzer
authors.forename: B S
authors.initials: BS
authors.lastname: Kuehne
authors.forename: J
authors.initials: J
authors.lastname: Tofighi
authors.forename: C
authors.initials: C
authors.lastname: Laske
authors.forename: E
authors.initials: E
authors.lastname: Stolz
authors.forename: F
authors.initials: F
authors.lastname: Blaes
authors.forename: K
authors.initials: K
authors.lastname: Voigt
authors.forename: H
authors.initials: H
authors.lastname: Traupe
authors.forename: M
authors.initials: M
authors.lastname: Kaps
authors.forename: P
authors.initials: P
authors.lastname: Oschmann
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology / Q000627:therapeutic use*; D000328:Adult; D015703:Antigens, CD / Q000276:immunology*; D015415:Biomarkers / Q000032:analysis; D015815:Cell Adhesion Molecules; D005260:Female; D006801:Humans; D007279:Injections, Subcutaneous; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000276:immunology* / Q000494:pharmacology / Q000627:therapeutic use*; D017493:Leukocyte Common Antigens / Q000276:immunology*; D016131:Lymphocyte Subsets; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology*; D011994:Recombinant Proteins; D012008:Recurrence
chemical_list: D000276:Adjuvants, Immunologic; D015703:Antigens, CD; D015415:Biomarkers; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D011994:Recombinant Proteins; D000068576:Interferon beta-1b; D016899:Interferon-beta; D017493:Leukocyte Common Antigens