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肺炎支原体的红细胞受体是Ii抗原型的唾液酸化寡糖。

Erythrocyte receptors for Mycoplasma pneumoniae are sialylated oligosaccharides of Ii antigen type.

作者信息

Loomes L M, Uemura K, Childs R A, Paulson J C, Rogers G N, Scudder P R, Michalski J C, Hounsell E F, Taylor-Robinson D, Feizi T

出版信息

Nature. 1984;307(5951):560-3. doi: 10.1038/307560a0.

DOI:10.1038/307560a0
PMID:6420710
Abstract

Among the pathological effects in man following infection with Mycoplasma pneumoniae is a transient autoimmune disorder characterized by the presence of high-titre erythrocyte autoantibodies (cold agglutinins). These autoantibodies are usually directed against the carbohydrate antigen termed I (ref. 3) which consists of a branched oligosaccharide. The mechanism by which the anti-I antibodies are elicited is unknown. However, sialic acid-containing receptors have been implicated in the adherence of M. pneumoniae to erythrocytes and other cell types, and both I and the related antigen i occur on erythrocytes in sialylated form: i is the predominant antigen on fetal erythrocytes and I is predominant in adults. Anti-I antibodies might arise in M. pneumoniae infection in response to a modification of the 'self' antigen-I as a result of its interaction with this agent. Here we report our study of the specificity of the interaction of M. pneumoniae with human erythrocytes. We found that this interaction is mediated by long chain oligosaccharides of sialic acid joined by alpha 2-3 linkage to the terminal galactose residues of poly-N-acetyllactosamine sequences of Ii antigen type.

摘要

人类感染肺炎支原体后的病理效应之一是一种短暂的自身免疫性疾病,其特征是存在高滴度的红细胞自身抗体(冷凝集素)。这些自身抗体通常针对一种称为I的碳水化合物抗原(参考文献3),它由一种分支寡糖组成。引发抗I抗体的机制尚不清楚。然而,含唾液酸的受体与肺炎支原体对红细胞及其他细胞类型的黏附有关,并且I和相关抗原i均以唾液酸化形式存在于红细胞上:i是胎儿红细胞上的主要抗原,而I在成人中占主导。抗I抗体可能在肺炎支原体感染时因“自身”抗原I与该病原体相互作用而发生修饰后产生。在此,我们报告了我们对肺炎支原体与人类红细胞相互作用特异性的研究。我们发现这种相互作用是由唾液酸的长链寡糖介导的,这些寡糖通过α2-3连接与Ii抗原型多聚N-乙酰乳糖胺序列的末端半乳糖残基相连。

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Erythrocyte receptors for Mycoplasma pneumoniae are sialylated oligosaccharides of Ii antigen type.肺炎支原体的红细胞受体是Ii抗原型的唾液酸化寡糖。
Nature. 1984;307(5951):560-3. doi: 10.1038/307560a0.
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