The αβ T cell response to self-glycolipids shows a novel mechanism of CD1b loading and a requirement for complex oligosaccharides
The αβ T cell response to self-glycolipids shows a novel mechanism of CD1b loading and a requirement for complex oligosaccharides
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DOI：
10.1016/s1074-7613(00)00025-x
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发表时间：
2000-08-01
期刊：
影响因子：
32.4
通讯作者：
De Libero, G
中科院分区：
文献类型：
--
作者：
Shamshiev, A;Donda, A;De Libero, G
T细胞识别脂多糖的结构基础仍有待阐明。我们描述了CD1b提出的对GM1神经节苷脂有反应的自身反应性T细胞。我们发现，糖鞘糖脂在中性pH下与细胞表面的CD1b结合，无需内化或加工即可识别。此外，可溶性GM1-CD1b复合体可刺激特定的T细胞。含有五个或五个以上糖的低聚糖基团需要构建用于TCR识别的最小表位。这提示了T细胞识别糖鞘糖脂的机制，其中大部分CD1b结合的配体暴露在外面。与CD1b的结合是一个高度可逆的过程，其他含神经酰胺的神经鞘糖脂取代GM1。这些非抗原性化合物起到阻滞剂的作用，可能会阻止体内有害的自身反应。
The structural basis for the T cell recognition of lipoglycans remains to be elucidated. We have described autoreactive T cells responsive to GM1 ganglioside presented by CD1b. We show that glycosphingolipids bind to CD1b on the cell surface at neutral pH and are recognized without internalization or processing. Furthermore, soluble GM1-CD1b complexes stimulate specific T cells. Oligosaccharide groups containing five or more sugars are required to build a minimal epitope for TCR recognition. This suggests a mechanism for T cell recognition of glycosphingolipids in which much of the CD1b-bound ligand is exposed. Binding to CD1b is a highly reversible process and other ceramide-containing glycosphingolipids displace GM1. These nonantigenic compounds act as blockers and may prevent harmful autoreactivity in vivo.