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
Objectives
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.
Results
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.
Conclusion
Our findings indicate that therapy
of multiple sclerosis with glatiramer acetate presumably involves the compensation
of altered apoptosis in T-helper lymphocytes.
© Munksgaard 2001