October 16, 2002
According to a study from Canada, "The efficacy of glatiramer acetate in multiple sclerosis (MS) is thought to involve the production of Th2 regulatory lymphocytes that secrete anti-inflammatory cytokines, however, other mechanisms cannot be excluded."
Given that activated T lymphocytes infiltrate into the CNS and become in close proximity to microglia," stated S. Chabot and colleagues, University of Calgary, "we evaluated whether glatiramer acetate affects the potential interaction between T cells and microglia.
"We report that the coculture of activated T lymphocytes with microglia led to the induction of several cytokines, and that these were reduced by glatiramer acetate treatment. Morphological transformation of bipolar/ramified microglia into an activated ameboid form was attenuated by glatiramer acetate." Chabot and coworkers concluded: "These results reveal a novel mechanism for glatiramer acetate: the impairment of activated T cells to effectively interact with microglia to produce cytokines. The net result of a noninflammatory milieu within the CNS, in spite of T-cell infiltration, may help account for the amelioration of disease activity in MS patients on glatiramer acetate therapy."
Chabot and coauthors published the results of their study in Multiple Sclerosis (Cytokine production in T lymphocyte-microglia interaction is attenuated by glatiramer acetate: a mechanism for therapeutic efficacy in multiple sclerosis. Mult Scler, 2002;8(4):299-306).
The corresponding author for this report is V.W. Yong, University Calgary, Neuroscience Research Group, Faculty of Medicine, Dept. of Clinical Neuroscience, 3330 Hospital Dr. NW, Calgary, AB T2N 4N1, Canada.
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The information in this article comes under the major subject areas of Immunology, Neurology, Multiple Sclerosis.
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