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Lymphocyte migration and multiple sclerosis: Relation with disease course and therapy
Author(s) -
Prat Alexandre,
AlAsmi Abdulla,
Duquette Pierre,
Antel Jack P.
Publication year - 1999
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(199908)46:2<253::aid-ana16>3.0.co;2-c
Subject(s) - glatiramer acetate , multiple sclerosis , medicine , lymphocyte , immunology , central nervous system , in vivo , biology , microbiology and biotechnology
Lymphocyte migration into the central nervous system is a central event in lesion formation in multiple sclerosis. By using a fibronectin‐coated membrane Boyden chamber assay, we observed that migration rates of immediately ex vivo lymphocytes from patients with relapsing–remitting, with or without concurrent clinical relapse, or with secondary progressive disease, were increased compared with healthy donors. Migration rates of lymphocytes from relapsing–remitting multiple sclerosis patients receiving either glatiramer acetate (Copaxone 20 mg daily) or interferon‐β1b (Betaseron 8 MIU, three times per week) were significantly reduced compared with untreated relapsing–remitting patients. In vitro treatment with interferon‐β1b (1,000 U/ml), but not glatiramer acetate (20 μg/ml), significantly reduced lymphocyte‐migration rates, suggesting that the effects of these two therapeutic agents on migration result from different mechanisms of actions. Interferon‐β1b acts, at least in part, by a direct effect on this cell property, whereas glatiramer acetate effects are indirect. Ann Neurol 1999;46:253–256