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Mechanism of demyelination and remyelination in multiple sclerosis
Author(s) -
Bando Yoshio
Publication year - 2020
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12576
Subject(s) - remyelination , multiple sclerosis , myelin , neuropathology , experimental autoimmune encephalomyelitis , oligodendrocyte , neuroscience , central nervous system , pathology , biology , mechanism (biology) , medicine , immunology , disease , philosophy , epistemology
Recent insights into its molecular neuropathology and immunology have provided a comprehensive overview of the pathology of multiple sclerosis (MS), including demyelination and axonal loss. To date, neuropathology in MS as the human autoimmune disease is considered to be mainly mediated by autoreactive leukocytes. By contrast, accumulating evidence has also suggested that the inflammation and tissue damage in MS and its animal model, experimental autoimmune encephalomyelitis, (EAE) is also critically regulated by glial cells in the central nervous system. However, the molecular mechanism of the glial cells‐mediated pathology of MS/EAE has not been fully understood. We examined the oligodendrocyte‐mediated demyelination and axonal injury. To address this issue, we established a new scanning electron microscopy analysis to observe ultrastructural myelin morphology. In addition, we focused on kallikrein 6, a serine protease, secreted by oligodendrocytes in the central nervous system and proposed a new molecular mechanism of kallikrein 6‐mediated demyelination. In this article, we discuss the pathological roles of oligodendrocytes in mouse models of EAE. We also highlight recent findings of abnormal myelin formation and axonal injury in EAE.