作者: Gustavo A. Nores , Ricardo D. Lardone , Romina Comín , María E. Alaniz , Ana L. Moyano
DOI: 10.1016/J.BBAGEN.2007.09.008
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摘要: Glycans are a class of molecules with high structural variability, frequently found in the plasma membrane facing extracellular space. Because these characteristics, glycans often considered as recognition involved cell social functions, and targets pathogenic factors. Induction anti-glycan antibodies is one early events immunological defense against bacteria that colonize body. this natural infection, recognizing variety bacterial sera adult humans animals. The immune response to restricted by self-tolerance, no self-glycans should exist normal subjects. However, structures closely related do exist, can lead production harmful anti-self antibodies. Normal human contain low-affinity anti-GM1 IgM-antibodies. Similar higher affinity or different isotype some neuropathy patients. Two hypotheses have been developed explain origin disease-associated According "molecular mimicry" hypothesis, similarity between GM1 Campylobacter jejuni lipopolysaccharide carrying GM1-like glycan cause Guillain-Barre syndrome associated IgG-antibodies. "binding site drift" IgM-antibodies disease originate through changes binding normally occurring We now present an "integrated" combining "mimicry" "drift" concepts, which satisfactorily explains most published data on