Microbiological and immunological aspects of Guillain-Barré syndrome

Guillain-Barré syndrome (GBS) is rare postinfection monophasic autoimmune disorder, which includes different clinical phenotypes of acute immune-mediated neuropathy. The symptoms may be caused by in ammatory demyelination, axonal degeneration, or both. Disease pathogenesis remains to be not clear, despite significant efforts in this field. Nevertheless certain progress in understanding of disease driving factors had been achieved, particularly in some points of association between the clinical phenotypes, the nature of antecedent infection and some types of circulating anti-ganglioside antibodies. It was shown the link between acute motor axonal neuropathy and antibodies to GM1, GD1a, GM1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the disialylated gangliosides GQ1b, GT1a, GD1b and GD3. In addition to clinical and serological studies, the origins and measurement of antiglycolipid antibodies and their relationships to similar carbohydrate structures on infectious organisms are discussed in the context of a molecular mimicry hypothesis. Despite these advances, considerable gaps in our knowledge persist, and it is likely that other factors are involved in GBS pathogenesis. This review highlights existing level of understanding and last updates on this topic.