Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate

Citation
O. Aktas et al., Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate, ACT NEUR SC, 104(5), 2001, pp. 266-270
Citations number
23
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ACTA NEUROLOGICA SCANDINAVICA
ISSN journal
00016314 → ACNP
Volume
104
Issue
5
Year of publication
2001
Pages
266 - 270
Database
ISI
SICI code
0001-6314(200111)104:5<266:MSMOAS>2.0.ZU;2-U
Abstract
Objectives - We investigated whether therapy of multiple sclerosis (MS) wit h glatiramer acetate (GA) involves the modulation of programmed cell death (apoptosis) in disease-relevant T-helper lymphocytes. Material and methods - Blood was drawn from 15 relapsing-remitting MS patients both before (base line) as well as 6, 12, and 18 weeks after GA therapy and from 15 healthy c ontrols. Detection of apoptosis was performed ill response to in vitro stim ulation with GA, myelin basic protein or medium alone. Results - T-helper l ymphocytes from untreated MS patients displayed an overall increased apopto sis susceptibility ill vitro, con pared to controls. During subsequent GA t herapy, apoptosis vulnerability of these T cells in MS patients significant ly declined under the initial baseline before treatment, and was finally eq ual in treated patients and controls. GA itself had no direct apoptosis-mod ulatory properties ill vitro. Conclusion - Our findings indicate that thera py of multiple sclerosis with glatiramer acetate presumably involves the co mpensation of altered apoptosis in T-helper lymphocytes.