More MS news articles for Nov 2001

Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate

Acta Neurologica Scandinavica 104 (5), 266-270
 O. Aktas (1), N. Ari (2), M. Rieks (2,3), V. Hoffmann (2), S. Schimrigk (2), H. Przuntek (2) and D. Pöhlau (4)
From  the
(1) Division of Neuroimmunology, Department of Neurology, Charité, Berlin, Germany,
(2) Department of Neurology, St Josef-Hospital, Ruhr-University Bochum, Germany,
(3) Department of Microbiology, Ruhr-University Bochum, Germany,
(4) Department of Neurology, Kamillusklinik, Asbach, Germany


We investigated whether therapy of multiple sclerosis (MS) with 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 (baseline) as well as 6, 12, and 18 weeks after GA therapy and from 15 healthy controls. Detection of apoptosis was performed in response to in vitro stimulation with GA, myelin basic protein or medium alone.


T-helper lymphocytes from untreated MS patients displayed an overall increased apoptosis susceptibility in vitro, compared to controls. During subsequent GA therapy, apoptosis vulnerability of these T cells in MS patients significantly declined under the initial baseline before treatment, and was finally equal in treated patients and controls. GA itself had no direct apoptosis-modulatory properties in vitro.


Our findings indicate that therapy of multiple sclerosis with glatiramer acetate presumably involves the compensation of altered apoptosis in T-helper lymphocytes.

© Munksgaard 2001