Chapter title |
Immunological expression of gangliosides in multiple sclerosis and in a demyelinating model disease in rabbits.
|
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Chapter number | 37 |
Book title |
Ganglioside Structure, Function, and Biomedical Potential
|
Published in |
Advances in experimental medicine and biology, January 1984
|
DOI | 10.1007/978-1-4684-1200-0_37 |
Pubmed ID | |
Book ISBNs |
978-1-4684-1202-4, 978-1-4684-1200-0
|
Authors |
Sela, B A, Offner, H, Konat, G, Lev-Ram, V, Cohen, O, Cohen, I R, Ben-Ami Sela, Halina Offner, Gregory Konat, Varda Lev-Ram, Oded Cohen, Irun R. Cohen, Sela, Ben-Ami, Offner, Halina, Konat, Gregory, Lev-Ram, Varda, Cohen, Oded, Cohen, Irun R. |
Abstract |
Accumulating evidence suggests that the process of demyelination in MS might involve an autoimmune response to one or more myelin components. A combination of myelin basic protein and myelin haptens was considered as possibly enhancing a cellular or humoral autoimmune reaction in MS. In line with this motion we have used an in-vitro E-rosette assay that correlates with in-vivo delayed hypersensitivity to demonstrate specific immunologic sensitivity of lymphocytes from MS patients to polysialogangliosides. A recent report that only lymphocytes from patients in relapse, but not in remission, are primed by gangliosides, underscores the relevance of the antigenic expression of gangliosides during the active pathological phase of the disease. The antigenic capacity of gangliosides to induce upon immunization a neurological disorder featured by demyelination in the CNS was demonstrated in rabbits. This and previous reports on the induction of peripheral demyelination in rabbits immunized with gangliosides will be further analyzed to gain insight on the possible role of these myelin lipid components as targets for an autoimmune mechanism in MS. |
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Geographical breakdown
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Demographic breakdown
Readers by professional status | Count | As % |
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Professor > Associate Professor | 2 | 50% |
Student > Postgraduate | 1 | 25% |
Unknown | 1 | 25% |
Readers by discipline | Count | As % |
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