Macrophages and Autoantibodies in Demyelinating Diseases
Myelin phagocytosis by macrophages has been an essential feature of demyelinating diseases in the central and peripheral nervous systems, including Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multiple sclerosis (MS). The discovery of autoantibodies, i...
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MDPI AG
2021-04-01
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| Online Access: | https://www.mdpi.com/2073-4409/10/4/844 |
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| author | Haruki Koike Masahisa Katsuno |
| author_facet | Haruki Koike Masahisa Katsuno |
| author_sort | Haruki Koike |
| collection | DOAJ |
| description | Myelin phagocytosis by macrophages has been an essential feature of demyelinating diseases in the central and peripheral nervous systems, including Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multiple sclerosis (MS). The discovery of autoantibodies, including anti-ganglioside GM1 antibodies in the axonal form of GBS, anti-neurofascin 155 and anti-contactin 1 antibodies in typical and distal forms of CIDP, and anti-aquaporin 4 antibodies in neuromyelitis optica, contributed to the understanding of the disease process in a subpopulation of patients conventionally diagnosed with demyelinating diseases. However, patients with these antibodies are now considered to have independent disease entities, including acute motor axonal neuropathy, nodopathy or paranodopathy, and neuromyelitis optica spectrum disorder, because primary lesions in these diseases are distinct from those in conventional demyelinating diseases. Therefore, the mechanisms underlying demyelination caused by macrophages remain unclear. Electron microscopy studies revealed that macrophages destroy myelin as if they are the principal players in the demyelination process. Recent studies suggest that macrophages seem to select specific sites of myelinated fibers, including the nodes of Ranvier, paranodes, and internodes, for the initiation of demyelination in individual cases, indicating that specific components localized to these sites play an important role in the behavior of macrophages that initiate myelin phagocytosis. Along with the search for autoantibodies, the ultrastructural characterization of myelin phagocytosis by macrophages is a crucial step in understanding the pathophysiology of demyelinating diseases and for the future development of targeted therapies. |
| first_indexed | 2024-03-10T12:30:19Z |
| format | Article |
| id | doaj.art-d6075ad52cff4d5496e98ab6e5f67ff6 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-10T12:30:19Z |
| publishDate | 2021-04-01 |
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| spelling | doaj.art-d6075ad52cff4d5496e98ab6e5f67ff62023-11-21T14:42:59ZengMDPI AGCells2073-44092021-04-0110484410.3390/cells10040844Macrophages and Autoantibodies in Demyelinating DiseasesHaruki Koike0Masahisa Katsuno1Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, JapanDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, JapanMyelin phagocytosis by macrophages has been an essential feature of demyelinating diseases in the central and peripheral nervous systems, including Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multiple sclerosis (MS). The discovery of autoantibodies, including anti-ganglioside GM1 antibodies in the axonal form of GBS, anti-neurofascin 155 and anti-contactin 1 antibodies in typical and distal forms of CIDP, and anti-aquaporin 4 antibodies in neuromyelitis optica, contributed to the understanding of the disease process in a subpopulation of patients conventionally diagnosed with demyelinating diseases. However, patients with these antibodies are now considered to have independent disease entities, including acute motor axonal neuropathy, nodopathy or paranodopathy, and neuromyelitis optica spectrum disorder, because primary lesions in these diseases are distinct from those in conventional demyelinating diseases. Therefore, the mechanisms underlying demyelination caused by macrophages remain unclear. Electron microscopy studies revealed that macrophages destroy myelin as if they are the principal players in the demyelination process. Recent studies suggest that macrophages seem to select specific sites of myelinated fibers, including the nodes of Ranvier, paranodes, and internodes, for the initiation of demyelination in individual cases, indicating that specific components localized to these sites play an important role in the behavior of macrophages that initiate myelin phagocytosis. Along with the search for autoantibodies, the ultrastructural characterization of myelin phagocytosis by macrophages is a crucial step in understanding the pathophysiology of demyelinating diseases and for the future development of targeted therapies.https://www.mdpi.com/2073-4409/10/4/844demyelinationelectron microscopymacrophageparanodepathogenesispathology |
| spellingShingle | Haruki Koike Masahisa Katsuno Macrophages and Autoantibodies in Demyelinating Diseases Cells demyelination electron microscopy macrophage paranode pathogenesis pathology |
| title | Macrophages and Autoantibodies in Demyelinating Diseases |
| title_full | Macrophages and Autoantibodies in Demyelinating Diseases |
| title_fullStr | Macrophages and Autoantibodies in Demyelinating Diseases |
| title_full_unstemmed | Macrophages and Autoantibodies in Demyelinating Diseases |
| title_short | Macrophages and Autoantibodies in Demyelinating Diseases |
| title_sort | macrophages and autoantibodies in demyelinating diseases |
| topic | demyelination electron microscopy macrophage paranode pathogenesis pathology |
| url | https://www.mdpi.com/2073-4409/10/4/844 |
| work_keys_str_mv | AT harukikoike macrophagesandautoantibodiesindemyelinatingdiseases AT masahisakatsuno macrophagesandautoantibodiesindemyelinatingdiseases |