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Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate
Author(s) -
Aktas O.,
Ari N.,
Rieks M.,
Hoffmann V.,
Schimrigk S.,
Przuntek H.,
Pöhlau D.
Publication year - 2001
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1034/j.1600-0404.2001.00125.x
Subject(s) - glatiramer acetate , multiple sclerosis , apoptosis , in vitro , immunology , medicine , myelin basic protein , oncology , endocrinology , myelin , biology , central nervous system , biochemistry
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.