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凋亡与自噬:在蜱-病原体相互作用中的最新认识。

Apoptosis and Autophagy: Current Understanding in Tick-Pathogen Interactions.

机构信息

Department of Entomology, University of Minnesota, St. Paul, MN, United States.

出版信息

Front Cell Infect Microbiol. 2022 Jan 27;12:784430. doi: 10.3389/fcimb.2022.784430. eCollection 2022.

DOI:10.3389/fcimb.2022.784430
PMID:35155277
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8829008/
Abstract

Tick-borne diseases are a significant threat to human and animal health throughout the world. How tick-borne pathogens successfully infect and disseminate in both their vertebrate and invertebrate hosts is only partially understood. Pathogens have evolved several mechanisms to combat host defense systems, and to avoid and modulate host immunity during infection, therefore benefitting their survival and replication. In the host, pathogens trigger responses from innate and adaptive immune systems that recognize and eliminate invaders. Two important innate defenses against pathogens are the programmed cell death pathways of apoptosis and autophagy. This Mini Review surveys the current knowledge of apoptosis and autophagy pathways in tick-pathogen interactions, as well as the strategies evolved by pathogens for their benefit. We then assess the limitations to studying both pathways and discuss their participation in the network of the tick immune system, before highlighting future perspectives in this field. The knowledge gained would significantly enhance our understanding of the defense responses in vector ticks that regulate pathogen infection and burden, and form the foundation for future research to identify novel approaches to the control of tick-borne diseases.

摘要

蜱传疾病是全球范围内对人类和动物健康的重大威胁。蜱传病原体如何成功感染和在脊椎动物和无脊椎动物宿主中传播仍部分未知。病原体已经进化出几种机制来对抗宿主防御系统,并在感染过程中避免和调节宿主免疫,从而有利于它们的存活和复制。在宿主中,病原体引发先天和适应性免疫系统的反应,识别并清除入侵者。针对病原体的两种重要先天防御是细胞凋亡和自噬的程序性细胞死亡途径。本综述调查了蜱-病原体相互作用中细胞凋亡和自噬途径的最新知识,以及病原体为自身利益而进化出的策略。然后,我们评估了研究这两条途径的局限性,并讨论了它们在蜱免疫系统网络中的参与情况,最后强调了该领域的未来展望。获得的知识将极大地增强我们对调节病原体感染和负担的载体蜱防御反应的理解,并为未来研究确定控制蜱传疾病的新方法奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ba4/8829008/35d95e124ccc/fcimb-12-784430-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ba4/8829008/3f5839550830/fcimb-12-784430-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ba4/8829008/35d95e124ccc/fcimb-12-784430-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ba4/8829008/3f5839550830/fcimb-12-784430-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ba4/8829008/35d95e124ccc/fcimb-12-784430-g002.jpg

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ATF6 enables pathogen infection in ticks by inducing and altering cholesterol dynamics.活化转录因子6通过诱导和改变胆固醇动态变化,使蜱虫能够发生病原体感染。
Proc Natl Acad Sci U S A. 2025 Jun 24;122(25):e2501045122. doi: 10.1073/pnas.2501045122. Epub 2025 Jun 17.
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protein of adhesion inhibits human urethral epithelial cells apoptosis via CypA/PI3K/AKT/mTOR-dependent autophagy.

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