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Brain immunohistopathology in a patient with autoimmune Glial Fibrillary acidic protein astrocytopathy
Journal article   Peer reviewed

Brain immunohistopathology in a patient with autoimmune Glial Fibrillary acidic protein astrocytopathy

Y. Shu, Y. Long, Y. Chang, R. Li, X. Sun, Y. Wang, Y. Huang, J. Li, J. Chen, Y. Yang, …
Neuroimmunomodulation, Vol.25(1), pp.1-6
2018
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Abstract

Background: Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is a novel meningoencephalomyelitis. However, the pathogenesis of this disease is unclear. We therefore examined a brain biopsy from a patient with autoimmune GFAP astrocytopathy by immunohistopathology. Methods: We examined brain biopsy sections from a patient with autoimmune GFAP astrocytopathy using hematoxylin and eosin (HE) and Luxol fast blue (LFB) staining, and immunostaining with antibodies for CD4, CD8, CD3, CD20, CD68, CD138, Neu-N, GFAP, myelin oligodendrocyte glycoprotein (MOG), and aquaporin-4 (AQP4). Results: HE staining revealed extensive inflammatory cells (marked lymphocytes) around brain vessels, and LFB showed no signs of demyelination or axon loss. Immunohistochemical analysis showed CD3+ and CD4+ T cells cuffing around brain vessels, accompanied by CD8+ T cells, CD20+ B cells, and CD138+ plasma cells, while some macrophages (CD68+) were scattered throughout the brain parenchyma. There was no loss of AQP4 or MOG expression in this patient, while GFAP was abundantly expressed. Conclusions: These findings suggest that inflammatory cells, including T cells, B cells, plasma cells, and macrophages, are involved in autoimmune GFAP astrocytopathy. Demyelination and astrocyte loss may not necessarily occur in this disease.

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Collaboration types
Domestic collaboration
International collaboration
Citation topics
1 Clinical & Life Sciences
1.203 Neuromuscular Disorders
1.203.1602 Limbic Encephalitis
Web Of Science research areas
Endocrinology & Metabolism
Immunology
Neurosciences
ESI research areas
Neuroscience & Behavior
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