CD45RA+ ICAM-3+ lymphocytes in interferon-β1b-treated and -untreated patients with relapsing–remitting multiple sclerosis.

Chatzimanolis N, Kraus J, Bauer R , Engelhardt B, Bregenzer T, Kuehne BS, Tofighi J, Laske C, Stolz E, Blaes F, Voigt K, Traupe H, Kaps M, Oschmann P. CD45RA+ ICAM-3+ lymphocytes in interferon-β1b-treated and -untreated patients with relapsing–remitting multiple sclerosis. Acta Neurol Scand 2004 DOI: 10.1111/j.1600-0404.2004.00346.x© Blackwell Munksgaard 2004.Multiple sclerosis (MS) is believed to be an autoimmune disease of the human central nervous system mediated by autoreactive T cells. Interferon-β1b (IFN-β1b) 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.Forty-eight patients with RRMS, 24 of them treated with recombinant IFN-β1b 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.We found a temporary increase in the CD45RA+ ICAM-3+ lymphocyte ratio in peripheral blood of both untreated and IFN-β1b-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.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-β1b treatment. [ABSTRACT FROM AUTHOR]