Correction to: Archeological neuroimmunology: resurrection of a pathogenic immune response from a historical case sheds light on human autoimmune encephalomyelitis and multiple sclerosis

Beltrán, Eduardo; Paunovic, Manuela; Gebert, David; Cesur, Emine; Jeitler, Markus; Höftberger, Romana; Malotka, Joachim; Mader, Simone; Kawakami, Naoto; Meinl, Edgar; Bradl, Monika; Dornmair, Klaus; Lassmann, Hans

doi:10.1007/s00401-021-02267-6

Cited by 11 publications

(2 citation statements)

References 44 publications

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“…172,173 A recent report demonstrated the pathogenicity of an antibody derived from the RNA of postmortem human brain tissue and showed similar demyelinating activity to a prototypical murinederived MOG Ab. 174 However, these studies use rodent-reactive antibodies which are only present in a minor proportion of MOGAD patients, with between 70 and 80% of human MOG Ab recognising a conformational epitope at position 42 of the extracellular domain of MOG where proline exists in humans as opposed to serine in rodents. 168,175 Autoantibody pathogenicity in a primate model has since been demonstrated in an in vivo macaque model in which complementdependent vacuolisation of myelin, lesion pathology, EAE and MOG Ab were observed after injection of recombinant human MOG.…”

Section: B Cells and Antibodiesmentioning

confidence: 99%

Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

et al. 2021

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Autoimmunity plays a significant role in the pathogenesis of demyelination. Multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are now recognised as separate disease entities under the amalgam of human central nervous system demyelinating disorders. While these disorders share inherent similarities, investigations into their distinct clinical presentations and lesion pathologies have aided in differential diagnoses and understanding of disease pathogenesis. An interplay of various genetic and environmental factors contributes to each disease, many of which implicate an autoimmune response. The pivotal role of the adaptive immune system has been highlighted by the diagnostic autoantibodies in NMOSD and MOGAD, and the presence of autoreactive lymphocytes in MS lesions. While a number of autoantigens have been proposed in MS, recent emphasis on the contribution of B cells has shed new light on the well-established understanding of T cell involvement in pathogenesis. This review aims to synthesise the clinical characteristics and pathological findings, discuss existing and emerging hypotheses regarding the aetiology of demyelination and evaluate recent pathogenicity studies involving T cells, B cells, and autoantibodies and their implications in human demyelination.

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Section: B Cells and Antibodiesmentioning

confidence: 99%

Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

et al. 2021

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“…Also, the precise mechanism of anti-MOG mediated demyelination is not clear, but may involve complement as suggested when using total IgG and organotypic brain slice cultures [39] and interactions with FcR as seen in humanized mice [40]. Intriguingly, reconstruction of the dominant antibody from an autopsy case with a pathology resembling multiple sclerosis following a misguided immunization with calf brain yielded a monoclonal antibody that recognized MOG and induced pathology together with T cells [41 ▪▪ ]. This supports the view that human MOG-IgG are pathogenic.…”

Section: Introductionmentioning

confidence: 99%

Pathomechanisms in demyelination and astrocytopathy: autoantibodies to AQP4, MOG, GFAP, GRP78 and beyond

Mader

Kümpfel

Meinl

2022

Current Opinion in Neurology

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Purpose of reviewThe purpose of this review is to highlight the recently emerging pathomechanisms of diseases associated with autoantibodies to AQP4, MOG, GFAP, GRP78 and further novel targets. We discuss novel biomarkers and therapeutic approaches.Recent findingsAlthough complement-mediated cytotoxicity (CDC) is regarded as the major effector mechanism for AQP4-IgG in neuromyelitis optica spectrum disorders (NMOSD), recent studies helped to understand the relevance of complement-independent effector mechanisms. For MOG-IgG mediated diseases the role of CDC is less clear. MOG-IgG may trigger a tightly controlled FcR and BTK-driven microglia proliferative response in MOG-antibody-associated diseases. Differences of antibody-mediated tissue damage may reflect differential response to therapy. In addition, antibodies to GFAP, GRP78 and further novel targets have been implicated in demyelination and astrocytopathy.SummaryElucidating the whole spectrum of effector functions in diseases mediated by AQP4-IgG and MOG-IgG and understanding the role of additional novel autoantibodies involved in demyelination and astrocytopathy may guide further novel treatment decisions.

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Kurt Jellinger 90: his contribution to neuroimmunology

et al. 2021

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This review honors Kurt Jellinger on his 90th birthday as one of the most outstanding neuropathologists, who has contributed immensely to neuroscience due to his vast experience and collection of excellently documented autopsy cases. Two of his many insightful reports are highlighted here. One report focuses on the pathogenesis of inflammatory demyelinating diseases and investigates the neuropathology in autopsy tissue of a patient, who developed an MS-like disease after repeated treatment with lyophilized bovine brain cells in 1958. More than 60 years later, after reinvestigation of the historic samples in 2015 and subsequent mRNA isolation, next generation sequencing and reconstruction of the antibody, we succeeded in identifying myelin oligodendrocyte glycoprotein (MOG) as the target antigen and provided the missing element between the pathomechanisms in classic EAE animal models and transfer of this disease process into humans. A second significant example of Kurt Jellinger’s contribution to neuroscience was a report on the role of MS in the development of Alzheimer's disease (AD), which found that AD pathology is present to the same extent in demyelinated and non-demyelinated cortical areas in MS and the incidence for AD pathology in elderly MS patients is comparable to the normal-aging population. This indicates that chronic inflammation in the MS cortex alone does not significantly predispose to the development of cortical AD pathology. These and other findings were only possible due to the broad collection of extremely well-defined material established by Kurt Jellinger, which ultimately continues to contribute to translational neuroscience, even decades later.

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Correction to: Archeological neuroimmunology: resurrection of a pathogenic immune response from a historical case sheds light on human autoimmune encephalomyelitis and multiple sclerosis

Abstract: Due to an error in the final editing of our manuscript the injection volume of intrathecal antibody application (page 72) was stated as 100 ml instead of 100 microliter.

Cited by 11 publications

References 44 publications

Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

Pathomechanisms in demyelination and astrocytopathy: autoantibodies to AQP4, MOG, GFAP, GRP78 and beyond

Kurt Jellinger 90: his contribution to neuroimmunology

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