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Pathogenese der multiplen Sklerose

  • P. Cabre
  • J. Oger
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  • 22 Downloads

Zusammenfassung

Heute wird allgemein die Auffassung vertreten, dass die multiple Sklerose (MS) durch eine fehlgeleitete Immunantwort gegen das zentrale Nervensystem (ZNS) verursacht wird. Das neuropathologische Substrat der aktiven MS-Läsion besteht vorwiegend aus einer Infiltration mononukleärer Zellen im Umfeld von Venolen. Dies führt zu einem multifokalen Myelinverlust und zu narbigen Läsionen; dabei kommt es zu einer Astrozytenproliferation und zu einem Verlust von Oligodendrozyten. Die verschiedenen Tiermodelle der MS, insbesondere die experimentelle Autoimmunenzephalomyelitis (EAE), haben stichhaltige Argumente geliefert, die für eine T-Lymphozyten-vermittelte Autoimmunkrankheit sprechen. Gleichwohl bleiben viele Fragen offen, was die Rolle von Umwelt-bzw. genetischen Faktoren bei der Entstehung der Erkrankung angeht. Infolge der jüngsten rasanten Fortschritte der Molekularbiologie und der immunologischen Grundlagenforschung konnten die unterschiedlichen Aktivierungsmechanismen der autoreaktiven T-Lymphozyten bei verschiedenen Antigenen (Ag) des ZNS genauer erkannt werden, doch wie wir sehen werden, stößt unser Verständnis der Pathogenese der Läsionen angesichts einer Vielzahl potentieller myelinhaltiger und sogar nicht myelinhaltiger Strukturbestandteile an Grenzen. Die Entwicklung der Kernspintomographie ermöglichte, den kritischen Mechanismus der Schädigung der Blut-Hirn-Schranke (BHS) am lebenden Patienten nachzuweisen.

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© Springer-Verlag Berlin Heidelberg 2003

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  • P. Cabre
  • J. Oger

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