Pathomechanisms in demyelination and astrocytopathy: autoantibodies to AQP4, MOG, GFAP, GRP78 and beyond.
Journal
Current opinion in neurology
ISSN: 1473-6551
Titre abrégé: Curr Opin Neurol
Pays: England
ID NLM: 9319162
Informations de publication
Date de publication:
01 06 2022
01 06 2022
Historique:
entrez:
8
6
2022
pubmed:
9
6
2022
medline:
10
6
2022
Statut:
ppublish
Résumé
The 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. Although 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. Elucidating 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.
Identifiants
pubmed: 35674086
doi: 10.1097/WCO.0000000000001052
pii: 00019052-202206000-00025
doi:
Substances chimiques
Aquaporin 4
0
Autoantibodies
0
Endoplasmic Reticulum Chaperone BiP
0
Immunoglobulin G
0
Banques de données
ClinicalTrials.gov
['NCT05063162']
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
427-435Informations de copyright
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
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