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MOG Antibody-Associated Disease and Thymic Hyperplasia: From the National Multiple Sclerosis Society Case Conference
Brigitte Hurtubise1, Elliot M Frohman1, Steven Galetta1
1From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco.
Abstract:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently described CNS inflammatory disorder that may manifest with optic neuritis, myelitis, seizures, and/or acute disseminated encephalomyelitis. While MOG-specific antibodies in patients with MOGAD are IgG1, a T-cell-dependent antibody isotype, immunologic mechanisms of this disease are not fully understood. Thymic hyperplasia can be associated with certain autoimmune diseases. In this report we describe a case of MOGAD associated with thymic hyperplasia in a young adult.
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