1 August 2002
Multiple Sclerosis, vol. 8, no. 4, pp. 299-306(8)
Chabot S; Yong FP; Le DM; Metz LM; Myles T; Yong VW
 Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada  Department of Clinical Neurosciences and Department of Oncology, Faculty of Medicine, University of Calgary, Calgary, Alberta, 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, we evaluated whether glatiramer acetate affects the potential interaction between T cells and microglia.
We report that the co-culture 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.
These results reveal a novel mechanism for glatiramer acetate: the impairment of activated T cells to effectively interact with microglia to produce cytokines.
net result of a non-inflammatory 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.
© 2002 ingenta