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DOI: 10.1055/s-2002-33657
Immuntherapie der multiplen Sklerose mit Glatiramerazetat (Copaxone®)
Wirkmechanismen und Ergebnisse aus TherapiestudienImmunotherapy of Multiple Sclerosis with Glatiramer AcetateMechanisms of Action and Results from Therapeutic TrialsPublikationsverlauf
Publikationsdatum:
26. September 2002 (online)
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Zusammenfasssung
Glatiramerazetat (GLAT; früher: Copolymer-1; Handelsname Copaxone®) hat von den modernen Immuntherapeutika bei multipler Sklerose (MS) die längste immunologische Vorgeschichte. Seine Wirkmechanismen werden auch heute noch nicht vollständig verstanden. In verschiedenen experimentellen Modellen gelang es durch GLAT akute und chronische Verläufe der experimentellen autoimmunen Enzephalomyelitis (EAE) zu therapieren. Zelluläre Untersuchungen an Tier und Mensch legen nahe, dass ein wesentliches Wirkprinzip in der Verschiebung der Immunantwort von sog. T-Helfer-1(TH1)-Mustern zu TH2-Mechanismen liegt. In kontrollierten klinischen Studien konnte die Wirkung von GLAT bei schubförmiger MS klinisch und kernspintomographisch nachgewiesen werden. Wir fassen in diesem Übersichtsartikel die vorliegenden Ergebnisse zu GLAT zusammen und diskutieren seinen Stellenwert bei der modernen MS-Therapie.
Abstract
Amongst immunomodulatory drugs used in multiple sclerosis (MS), glatiramer acetate (GLAT; former name: Copolymer-1; trademark Copaxone) has the longest history. Even today its mechanisms of action are only incompletely understood. GLAT has shown therapeutic efficacy in diverse models of experimental autoimmune encephalomyelitis (EAE). At the cellular level GLAT induces a shift from TH1 to TH2 cytokines. Therapeutic efficacy in relapsing-remitting MS patients has been proven by controlled clinical studies. Here we review current aspects of GLAT therapy and discuss its role in immunomodulatory treatment of MS.
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Prof. Dr. Ralf Gold
Neurologische Universitätsklinik
Josef-Schneider-Straße 11
97080 Würzburg
eMail: r.gold@mail.uni-wuerzburg.de