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鼠疫耶尔森菌LPS结构变异机制及其免疫逃逸功能研究进展

冯文静 张源 杜宗敏

中国人兽共患病学报2024,Vol.40Issue(9):860-866,7.
中国人兽共患病学报2024,Vol.40Issue(9):860-866,7.DOI:10.3969/j.issn.1002-2694.2024.00.134

鼠疫耶尔森菌LPS结构变异机制及其免疫逃逸功能研究进展

Advances in lipopolysaccharide structural variations and immune escape in Yersinia pestis

冯文静 1张源 2杜宗敏2

作者信息

  • 1. 牡丹江医学院公共卫生学院,牡丹江 157011
  • 2. 军事科学院军事医学研究院微生物流行病研究所,病原微生物生物安全全国重点实验室,北京 100071
  • 折叠

摘要

Abstract

Plague,caused by Yersinia pestis,is a zoonotic disease that infects both humans and animals.Y.pestis not only encodes various virulence factors that can disrupt host immune signaling but also can modify its lipopolysaccharide(LPS)struc-ture,thereby evading host immune surveillance and potently suppressing the host's immune response,in an important molecu-lar mechanism underlying its high pathogenicity.The LPS of Y.pestis lacks an O antigen,and its lipid A structure possesses a unique temperature transition regulatory mechanism.At different temperatures,Y.pestis forms lipid A with different numbers of acyl side chains,which plays a pivotal role in the evasion of host innate immune recognition and clearance.Here,we present a comprehensive review of research progress in the biosynthetic regulation,structural variation,and immune escape mechanism of Y.pestis LPS,to provide a reference for the study of the molecular mechanisms of pathogens using LPS structural modifica-tions to elude host innate immune defenses.

关键词

鼠疫菌/脂多糖/免疫逃逸

Key words

Yersinia pestis/lipopolysaccharide(LPS)/immune escape

分类

医药卫生

引用本文复制引用

冯文静,张源,杜宗敏..鼠疫耶尔森菌LPS结构变异机制及其免疫逃逸功能研究进展[J].中国人兽共患病学报,2024,40(9):860-866,7.

基金项目

Supported by the State Key Laboratory of Pathogen and Biosecurity(No.SKLPBS2211) 病原微生物生物安全全国重点实验室自主课题(No.SKLPBS2211) (No.SKLPBS2211)

中国人兽共患病学报

OA北大核心CSTPCD

1002-2694

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