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Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in the common marmoset reflects the immunopathology of pattern II multiple sclerosis lesionsDepartment of Neuropathology, Georg-August University Göttingen, Göttingen, Germany
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany, Institut für Multiple-Sklerose-Forschung, Bereich Humanmedizin der Universität Göttingen und Gemeinnützige Hertie-Stiftung, Göttingen, Germany, Department of Neurology, Georg-August University Göttingen, Göttingen, Germany
Department of Neuropathology, Georg-August University Göttingen, Göttingen, Germany
Department of Neuropathology, Georg-August University Göttingen, Göttingen, Germany, Institut für Multiple-Sklerose-Forschung, Bereich Humanmedizin der Universität Göttingen und Gemeinnützige Hertie-Stiftung, Göttingen, Germany, wbrueck{at}med.uni-goettingen.de Pathomorphological studies described pathological heterogeneity in patients with multiple sclerosis (MS). Different effector mechanisms might therefore be responsible for lesion formation in MS. The present report shows that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in common marmoset monkeys reflects one specific lesional subtype of MS, namely MS pattern II lesions with antibody/complement-mediated damage. MOG-induced EAE in marmoset monkeys will, therefore, provide an ideal model for therapeutic approaches directed against B-cell/antibody/complement in MS.
Key Words: common marmoset EAE multiple sclerosis
Multiple Sclerosis, Vol. 12, No. 4,
369-374 (2006) This article has been cited by other articles:
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