LC3-Associated Phagocytosis in Bacterial Infection

被引：18

作者：

Yuan, Jin ^{[1
]}

Zhang, Qiuyu ^{[1
]}

Chen, Shihua ^{[1
]}

Yan, Min ^{[1
]}

Yue, Lei ^{[2
]}

机构：

[1] Kunming Med Univ, Fac Basic Med Sci, Dept Pathogen Biol & Immunol, Kunming 650500, Yunnan, Peoples R China

[2] Chinese Acad Med Sci & Peking Union Med Coll, Inst Med Biol, Kunming 650118, Yunnan, Peoples R China

来源：

PATHOGENS | 2022年 / 11卷 / 08期

基金：

中国国家自然科学基金;

关键词：

LC3-associated phagocytosis; bacterial infection; phagocyte; immune evasion; III SECRETION SYSTEM; MYCOBACTERIUM-TUBERCULOSIS; LISTERIA-MONOCYTOGENES; BURKHOLDERIA-PSEUDOMALLEI; LC3; RECRUITMENT; STAPHYLOCOCCUS-AUREUS; NADPH OXIDASE; HOST-DEFENSE; YERSINIA-PSEUDOTUBERCULOSIS; NONCANONICAL AUTOPHAGY;

D O I：

10.3390/pathogens11080863

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

LC3-associated phagocytosis (LAP) is a noncanonical autophagy process reported in recent years and is one of the effective mechanisms of host defense against bacterial infection. During LAP, bacteria are recognized by pattern recognition receptors (PRRs), enter the body, and then recruit LC3 onto a single-membrane phagosome to form a LAPosome. LC3 conjugation can promote the fusion of the LAPosomes with lysosomes, resulting in their maturation into phagolysosomes, which can effectively kill the identified pathogens. However, to survive in host cells, bacteria have also evolved strategies to evade killing by LAP. In this review, we summarized the mechanism of LAP in resistance to bacterial infection and the ways in which bacteria escape LAP. We aim to provide new clues for developing novel therapeutic strategies for bacterial infectious diseases.

引用

页数：19

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