Modelling MOG antibody-associated disorder and neuromyelitis optica spectrum disorder in animal models: Spinal cord manifestations

Jana Remlinger; Maud Bagnoud; Ivo Meli; Marine Massy; Christopher Linington; Andrew Chan; Jeffrey L Bennett; Robert Hoepner; Volker Enzmann; Anke Salmen

doi:10.1016/j.msard.2023.104892

Modelling MOG antibody-associated disorder and neuromyelitis optica spectrum disorder in animal models: Spinal cord manifestations

Mult Scler Relat Disord. 2023 Oct:78:104892. doi: 10.1016/j.msard.2023.104892. Epub 2023 Jul 17.

Authors

Affiliations

¹ Department of Neurology, Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Bern, 3010, Switzerland; Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, 3010, Switzerland.
² Department of Neurology, Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Bern, 3010, Switzerland.
³ Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, G12 8TA, UK.
⁴ Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, United States of America.
⁵ Department of Ophthalmology, Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Bern, 3010, Switzerland.
⁶ Department of Neurology, Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Bern, 3010, Switzerland. Electronic address: anke.salmen@rub.de.

PMID: 37499337
DOI: 10.1016/j.msard.2023.104892

Abstract

Antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) or aquaporin 4 (AQP4-IgG) are associated with CNS inflammatory disorders. We directly compared MOG_35-55-induced experimental autoimmune encephalomyelitis exacerbated by MOG- and AQP4-IgG (versus isotype IgG, Iso-IgG). Disease severity was highest after MOG-IgG application. MOG- and AQP4-IgG administration increased disease incidence compared to Iso-IgG. Inflammatory lesions appeared earlier and with distinct localizations after AQP4-IgG administration. AQP4 intensity was more reduced after AQP4- than MOG-IgG administration at acute disease phase. The described models are suitable for comparative analyses of pathological features associated with MOG- and AQP4-IgG and the investigation of therapeutic interventions.

Keywords: AQP4-IgG; Experimental autoimmune encephalomyelitis; MOG antibody-associated disorder; MOG-IgG; Neuromyelitis optica spectrum disorder.