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脂质A增强脂质体包被霍乱毒素的黏膜免疫原性

Enhancement by lipid A of mucosal immunogenicity of liposome-associated cholera toxin.

作者信息

Pierce N F, Sacci J B, Alving C R, Richardson E C

出版信息

Rev Infect Dis. 1984 Jul-Aug;6(4):563-6. doi: 10.1093/clinids/6.4.563.

DOI:10.1093/clinids/6.4.563
PMID:6474016
Abstract

Two methods that might enhance the mucosal immunogenicity of a protein antigen, cholera toxin (CT), were studied in rats: association of CT with liposomes, and coadministration of CT with lipid A. Enteric priming by CT was not enhanced when the antigen was trapped within liposomes or bound to their surface via GM1 ganglioside, nor was it improved when CT was mixed with lipid A or with liposomes containing lipid A. However, lipid A did enhance priming by liposome-associated CT when the lipid A was incorporated into CT-bearing liposomes. It is concluded that lipid A can act as an adjuvant for a local IgA response to a mucosally applied antigen, at least when lipid A and the antigen are associated on a liposome carrier.

摘要

在大鼠中研究了两种可能增强蛋白质抗原霍乱毒素(CT)黏膜免疫原性的方法:CT与脂质体结合,以及CT与脂多糖A共同给药。当抗原被困在脂质体内或通过GM1神经节苷脂结合到其表面时,CT的肠道启动作用并未增强,当CT与脂多糖A或含有脂多糖A的脂质体混合时也没有改善。然而,当脂多糖A掺入含CT的脂质体中时,脂多糖A确实增强了脂质体相关CT的启动作用。得出的结论是,脂多糖A可以作为黏膜应用抗原的局部IgA反应的佐剂,至少当脂多糖A和抗原在脂质体载体上结合时是这样。

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