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以及脂多糖变异在固有免疫逃避中的作用。

and the Role of Lipopolysaccharide Variation in Innate Immune Evasion.

机构信息

School of Science, RMIT University, Melbourne, VIC, Australia.

ZiP Diagnostics, Collingwood, VIC, Australia.

出版信息

Front Immunol. 2022 May 13;13:868225. doi: 10.3389/fimmu.2022.868225. eCollection 2022.

DOI:10.3389/fimmu.2022.868225
PMID:35634347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9136243/
Abstract

is an important human pathogen that infects half the human population and can lead to significant clinical outcomes such as acute and chronic gastritis, duodenal ulcer, and gastric adenocarcinoma. To establish infection, employs several mechanisms to overcome the innate and adaptive immune systems. can modulate interleukin (IL) secretion and innate immune cell function by the action of several virulence factors such as VacA, CagA and the type IV secretion system. Additionally, can modulate local dendritic cells (DC) negatively impacting the function of these cells, reducing the secretion of immune signaling molecules, and influencing the differentiation of CD4 T helper cells causing a bias to Th1 type cells. Furthermore, the lipopolysaccharide (LPS) of displays a high degree of phase variation and contains human blood group carbohydrate determinants such as the Lewis system antigens, which are proposed to be involved in molecular mimicry of the host. Lastly, the group of outer membrane proteins such as BabA play an important role in attachment and interaction with host Lewis and other carbohydrate antigens. This review examines the various mechanisms that utilises to evade the innate immune system as well as discussing how the structure of the LPS plays a role in immune evasion.

摘要

幽门螺杆菌是一种重要的人类病原体,感染了半数的人类人口,可导致严重的临床后果,如急性和慢性胃炎、十二指肠溃疡和胃腺癌。为了建立感染,幽门螺杆菌采用了几种机制来克服先天和适应性免疫系统。幽门螺杆菌可以通过 VacA、CagA 和 IV 型分泌系统等几种毒力因子来调节白细胞介素(IL)的分泌和先天免疫细胞的功能。此外,幽门螺杆菌还可以负调控局部树突状细胞(DC),降低这些细胞的功能,减少免疫信号分子的分泌,并影响 CD4 T 辅助细胞的分化,导致 Th1 型细胞的偏向。此外,幽门螺杆菌的脂多糖(LPS)显示出高度的相变异和含有人类血型碳水化合物决定簇,如 Lewis 系统抗原,据推测这些抗原参与了宿主的分子模拟。最后,外膜蛋白组如 BabA 等在附着和与宿主 Lewis 及其他碳水化合物抗原相互作用中起着重要作用。本文综述了幽门螺杆菌逃避先天免疫系统的各种机制,并讨论了 LPS 的结构如何在免疫逃避中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/0fed6d0d3f67/fimmu-13-868225-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/4bb62253f6ea/fimmu-13-868225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/c8ccb81f27ba/fimmu-13-868225-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/0fed6d0d3f67/fimmu-13-868225-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/4bb62253f6ea/fimmu-13-868225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/c8ccb81f27ba/fimmu-13-868225-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/9136243/0fed6d0d3f67/fimmu-13-868225-g003.jpg

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