Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK.
Trends Immunol. 2013 Sep;34(9):453-9. doi: 10.1016/j.it.2013.05.001. Epub 2013 Jun 13.
Autoantibodies to glycans present on glycolipids mediate the postinfectious paralytic disease, Guillain-Barré syndrome (GBS). These glycans are also found on lipo-oligosaccharides (LOSs) of GBS-inducing microbes, suggesting molecular mimicry as a mechanism for disease induction. How B lymphocyte tolerance to self-glycans is regulated during the initiation phase of the disease is currently under investigation. The discovery of antiglycolipid antibodies that bind to heteromeric glycolipid complexes has generated new insights in this field. Heteromeric complexes are structurally distinct glycolipids that interact to form new molecular shapes capable of either enhancing or attenuating recognition by autoantibodies. Although the principles emerging from this phenomenon have a substantial impact on diagnostics methods, they also raise intriguing questions about the diversity of innate antibody repertoires, mechanisms of tolerance, and autoantibody targeting of neural membranes.
自身抗体与糖脂上的聚糖结合可介导感染后瘫痪性疾病，格林-巴利综合征（GBS）。这些聚糖也存在于诱导 GBS 的微生物的脂寡糖（LOS）上，提示分子模拟是疾病诱导的一种机制。目前正在研究在疾病起始阶段如何调节 B 淋巴细胞对自身聚糖的耐受性。发现与异质糖脂复合物结合的抗糖脂抗体为该领域提供了新的见解。异质复合物是结构上不同的糖脂，相互作用形成新的分子形状，能够增强或减弱自身抗体的识别。尽管这一现象所揭示的原理对诊断方法有重大影响，但它们也提出了关于先天抗体库多样性、耐受机制以及神经膜自身抗体靶向的有趣问题。
