Literature DB >> 11696019

Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate.

O Aktas1, N Ari, M Rieks, V Hoffmann, S Schimrigk, H Przuntek, D Pöhlau.   

Abstract

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.

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Year:  2001        PMID: 11696019     DOI: 10.1034/j.1600-0404.2001.00125.x

Source DB:  PubMed          Journal:  Acta Neurol Scand        ISSN: 0001-6314            Impact factor:   3.209


  1 in total

1.  Glatiramer acetate induces pro-apoptotic mechanisms involving Bcl-2, Bax and Cyt-c in peripheral lymphocytes from multiple sclerosis patients.

Authors:  M Ruggieri; C Avolio; S Scacco; C Pica; A Lia; G B Zimatore; S Papa; P Livrea; M Trojano
Journal:  J Neurol       Date:  2005-09-30       Impact factor: 4.849

  1 in total

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