Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study
Autor: | Mari Yoshida, Teppei Komatsu, Monika Bradl, Kiyotaka Nakamagoe, Tatsuro Misu, Ichiro Nakashima, Masashi Aoki, Hiroshi Kuroda, Kazuo Fujihara, Koichi Narikawa, Hiroyoshi Suzuki, Toshimasa Ikeda, Hans Lassmann, Hiroya Nishida, Kimihiko Kaneko, Takashi Komori, Morinobu Seki, Yoshiki Takai, Shuhei Nishiyama, Hirohiko Ono, Norio Chihara, Satoko Tsuchida, Toshiyuki Takahashi |
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Rok vydání: | 2020 |
Předmět: |
Adult
Male 0301 basic medicine Pathology medicine.medical_specialty Adolescent Myelitis Demyelinating Autoimmune Diseases CNS Autoantigens Myelin oligodendrocyte glycoprotein Young Adult 03 medical and health sciences Myelin 0302 clinical medicine medicine Demyelinating disease Humans Optic neuritis Child Autoantibodies Neuromyelitis optica biology business.industry Multiple sclerosis Brain Middle Aged medicine.disease 030104 developmental biology medicine.anatomical_structure Acute disseminated encephalomyelitis biology.protein Female Myelin-Oligodendrocyte Glycoprotein Neurology (clinical) business 030217 neurology & neurosurgery |
Zdroj: | Brain. 143:1431-1446 |
ISSN: | 1460-2156 0006-8950 |
Popis: | Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis. So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. In this study, we immunohistochemically analysed biopsied brain tissues from 11 patients with MOG antibody-associated disease and other inflammatory demyelinating diseases. Patient median onset age was 29 years (range 9–64), and the median interval from attack to biopsy was 1 month (range 0.5–96). The clinical diagnoses were ADEM (n = 2), MDEM (n = 1), multiple brain lesions without encephalopathy (n = 3), leukoencephalopathy (n = 3) and cortical encephalitis (n = 2). All these cases had multiple/extensive lesions on MRI and were oligoclonal IgG band-negative. Most demyelinating lesions in 10 of 11 cases showed a perivenous demyelinating pattern previously reported in ADEM (153/167 lesions) and a fusion pattern (11/167 lesions) mainly in the cortico-medullary junctions and white matter, and only three lesions in two cases showed confluent demyelinated plaques. In addition, 60 of 167 demyelinating lesions (mainly in the early phase) showed MOG-dominant myelin loss, but relatively preserved oligodendrocytes, which were distinct from those of AQP4 antibody-positive NMOSD exhibiting myelin-associated glycoprotein-dominant oligodendrogliopathy. In MOG antibody-associated diseases, MOG-laden macrophages were found in the perivascular spaces and demyelinating lesions, and infiltrated cells were abundant surrounding multiple blood vessels in and around the demyelinating lesions, mainly consisting of macrophages (CD68; 1814 ± 1188 cells/mm2), B cells (CD20; 468 ± 817 cells/mm2), and T cells (CD3; 2286 ± 1951 cells/mm2), with CD4-dominance (CD4+ versus CD8+; 1281 ± 1196 cells/mm2 versus 851 ± 762 cells/mm2, P |
Databáze: | OpenAIRE |
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