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Gangliosides as targets for autoimmune injury to the nervous system Willison HJJ Neurochem 2007[Nov]; 103 Suppl 1 (ä): 143-9Immune responses directed towards gangliosides and their microbial mimics are important mediators of several subtypes of acute post-infectious autoimmune neuropathy, collectively referred to as the Guillain-Barre syndromes. In this diverse group of paralytic syndromes, the immunopathology is in a proportion of cases characterised by anti-ganglioside antibody deposits, accompanied by inflammatory destruction of both axonal and glial components within the PNS. By gaining an understanding of the immunological mechanisms underlying these pathological pathways, it should be possible to select the correct targets for therapeutic intervention. Recent years has seen particular progress in our understanding of the basis for, and immunological consequences of molecular mimicry between gangliosides and microbial glycans, the relationships between ganglioside antibody specificity and different clinical phenotypes of GBS, the pathological basis for antibody-mediated nerve injury and the testing of intervention strategies in pre-clinical models. The focus of this mini-review is to provide a brief background to this field, summarise a selection of recent highlights focused on our own research, identify areas of outstanding knowledge and present data that supports novel therapeutic approaches based on the latest experimental findings.|*Molecular Mimicry/physiology[MESH]|Animals[MESH]|Autoantibodies/metabolism[MESH]|Autoimmune Diseases of the Nervous System/*immunology/therapy[MESH]|Gangliosides/*immunology[MESH]|Guillain-Barre Syndrome/immunology/pathology/physiopathology[MESH]|Humans[MESH]|Models, Biological[MESH] |
