In:
Clinical and Experimental Neuroimmunology, Wiley, Vol. 9, No. 1 ( 2018-02), p. 65-74
Abstract:
The pathogenesis of chronic inflammatory demyelinating polyneuropathy ( CIDP ) is composed of cellular and humoral immunities. Macrophages might play a crucial role in cellular immunity. In addition, autoantibodies participate in the pathogenesis of CIDP . To date, various autoantibodies have been reported to affect peripheral nerve myelin. Although antibodies to glycolipids are frequently identified in Guillain‐Barré syndrome and closely related to the development of neuropathies, these are detected in only a small percentage of CIDP instances. Among glycolipids, sialosylneolactotetraosylceramide ( LM 1) is predominantly localized in human peripheral nerve myelin. LM 1‐related antibodies (e.g. anti‐ LM 1, GM1/ LM 1 and GD 1b/ LM 1 antibodies) are detected in some patients with CIDP and Guillain‐Barré syndrome. CIDP patients with those antibodies frequently present ataxia, but rarely have cranial nerve deficits; these features are associated with the localization of LM 1, which is more abundant in the dorsal root than the cranial nerves. In immunoglobulin M paraproteinemic neuropathies, except for the anti‐myelin‐associated glycoprotein neuropathies, antibodies to glycolipids with disialosyl residues, such as GD 1b and GQ 1b, are also detected on occasion. Notably, this feature is clinically characterized by chronic ataxic neuropathy, ophthalmoplegia, immunoglobulin M paraprotein, cold agglutinins and disialosyl antibodies. Such clinical features are related to the localization of GD 1b or GQ 1b in human peripheral nerves. Overall, these correlations suggest a direct involvement of the antibodies in the pathogenesis of those aforementioned neuropathies.
Type of Medium:
Online Resource
ISSN:
1759-1961
,
1759-1961
DOI:
10.1111/cen3.2018.9.issue-1
Language:
English
Publisher:
Wiley
Publication Date:
2018
detail.hit.zdb_id:
2508135-4
