Abstract
Identification and characterization of antigens present at the human peripheral nerve is a great challenge in the field of neuroimmunology. The latest investigations are focused on the understanding of the biology of glycoconjugates present at the peripheral nerve, and their immunological reactivity. Increased titers of antibodies that recognize carbohydrate determinants of glycoconjugates (glycolipids and glycoproteins) are associated with distinct neuropathic syndromes. There is considerable cross-reactivity among anti-ganglioside antibodies, resulting from shared oligosaccharide epitopes, possibly explaining the overlap in syndromes observed in many affected patients. Sera from patients with neuropathies (GBS, chronic inflammatory demielynating polyneuropathy - CIDP, multifocal motor neuropathy - MMN), cross-react with glycoproteins isolated from human peripheral nerve and from Campylobacter jejuni O:19. The frequency of occurrence of antibodies against these glycoproteins is different, depending of the type of neuropathy. Identification of the cross-reactive glycoproteins and possible additional auto antigens could be useful in laboratory evaluation of peripheral neuropathies and help to develop a more effective therapeutic approach.
Highlights
Autoimmune neuropathies are described by presence of symptoms of weakness, sensory loss and autonomic dysfunctions as a consequence of immune mediated damage of peripheral nerve
These include myelin proteins myelin protein zero (P0), myelin -associated glycoprotein (MAG), peripheral myelin protein 2 (P2), peripheral myelin protein 22 (PMP22) and other myelin specific proteins that have an important role in myelin formation and in mediating autoimmune peripheral nerve disease (Quarles 1989, Hughes and Cornblath, 2005, Khalili-Shirazi et al, 1993, Quarles et al, 1990, Gabriel et al, 2000, Allen et al, 2005)
Results of our study revealed structural similarity in oligosaccharide portion and immunoreactivity of the glycoproteins isolated from peripheral nerve and C. jejuni, indicating that they are potentially cross-reactive determinants and may contribute to the development of GBS associated with antecedent C. jejuni infection (Poceva-Panovska et al, 2011)
Summary
Autoimmune neuropathies are described by presence of symptoms of weakness, sensory loss and autonomic dysfunctions as a consequence of immune mediated damage of peripheral nerve. From the clinical point of view, autoimmune neuropathies may have acute onset and monophasic course (Guillian-Barré syndrome - GBS and its variants), or chronic slow progressive or relapsing clinical course The subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN) and Miller Fisher syndrome (MFS). AIDP is characterized by primary demyelination, while AMAN is characterized by primary axonal degeneration of the peripheral nerves developed trough noninflammatory complement dependent mechanism mediated by antibodies MFS is characterized by an acute onset of ataxia, areflexia and ophtalmoplegia (Fisher 1956) All of these GBS variants have CSF finding characterized by increased protein level and normal cell count (albumino-cytological dissociation) and may have a detectable spectrum of serum antiganglioside antibodies. The muscle weakness related to individual motor nerve is associated with motor conduction block, at site distinct from common entrapment or compression syndromes (Ghosh et al, 2005; van der Meché et al, 1995; Willison and Yuki, 2002)
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