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Time-course analysis of CD25 and HLA-DR expression on lymphocytes in interferon-ß1b-treated multiple sclerosis patients

Department of Neurological and Psychiatrical Sciences, Second Neurological Clinic, University of Padua, Italy

S Sivieri

Department of Neurological and Psychiatrical Sciences, Second Neurological Clinic, University of Padua, Italy

M Buttarello

Laboratory of Clinical Chemistry, ULS-16, Padua

A Facchinetti

Department of Oncological and Surgical Sciences, University of Padua, Italy

P Perini

Department of Neurological and Psychiatrical Sciences, Second Neurological Clinic, University of Padua, Italy

P Gallo

Department of Neurological and Psychiatrical Sciences, Second Neurological Clinic, University of Padua, Italy

To identify immunological markers that could be used to monitor relapsing-remitting multiple sclerosis (RRMS) course/activity during interferon beta 1b (IFNß1b) therapy, we longitudinally studied HLA-DR and CD25 expression by T lymphocytes in 15 IFNß1b-treated RRMS patients. Peripheral blood T cell subsets were analysed before therapy (T0), and after 1 (T1), 2 (T2), 3 (T3), 6 (T4) and 12 (T5) months after therapy initiation. HLADR expression and the CD3+HLA-DR+ T cell number showed a peculiar trend in almost all (14/15) the patients: a significant decrease at T1 and T2 followed by a return to pre-treatment levels from T3 to T5. At T1 and T2, eight patients showed an up-regulation of CD25 on CD4, as well as an increase in the CD4+CD25+ cell number. However, a marked, significant reduction of this T cell subset was observed in all the patients at T3, followed by the progressive return to pre-treatment values from T4 to T5. All the patients developed anti-IFNß1b `binding' antibodies within the first three months of therapy. Our findings demonstrate that: (1) the expression of HLA-DR and CD25 on T cells, as well as the number of circulating CD3+HLA-DR+ and CD4+CD25+ cells, are only transiently reduced in vivo in IFNß1b-treated RRMS patients, (2) the expression of HLA-DR and CD25 on T lymphocytes cannot be used to monitor MS course/activity during IFNß1b therapy, (3) the long-lasting beneficial effect of IFNß1b on RRMS reported in the literature cannot be explained by the down-regulation of MHC class II antigens and/or interleukin-2 receptor expression induced by this cytokine.

Key Words: multiple sclerosis • interferon beta 1b • lymphocyte subsets • HLA-DR • CD4 • CD25

Multiple Sclerosis, Vol. 4, No. 3, 174-177 (1998)
DOI: 10.1177/135245859800400316


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