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

Shu, Y., Long, Y., Chang, Y., Li, R., Sun, X., Wang, Y., Huang, Y., Li, J., Chen, J., Yang, Y., Lu, Z., Hu, X., Kermode, A.G. and Qiu, W. (2018) Brain immunohistopathology in a patient with autoimmune Glial Fibrillary acidic protein astrocytopathy. Neuroimmunomodulation . In Press.

Link to Published Version: https://doi.org/10.1159/000488879
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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.

Item Type: Journal Article
Publisher: Karger
Copyright: © 2018 S. Karger AG, Basel
URI: http://researchrepository.murdoch.edu.au/id/eprint/41452
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