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.