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它通过释放细胞外囊泡来逃避宿主固有免疫，激活 TLR2-AKT 信号通路。

evades host innate immunity by releasing extracellular vesicles to activate TLR2-AKT signaling pathway.

机构信息

Key Laboratory of Zoonosis Research, Ministry of Education; College of Veterinary Medicine, Jilin University, Changchun, China.

出版信息

Virulence. 2021 Dec;12(1):2017-2036. doi: 10.1080/21505594.2021.1959495.

DOI:10.1080/21505594.2021.1959495
PMID:34348595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8344757/
Abstract

Surra, one of the most important animal diseases with economic consequences in Asia and South America, is caused by . However, the mechanism of immune evasion by has not been extensively studied. In the present study, extracellular vesicles (TeEVs) were characterized and the role of TeEVs in infection were examined. The results showed that and TeEVs could activate TLR2-AKT pathway to inhibit the secretions of IL-12p40, IL-6, and TNF-α in mouse BMDMs. TLR2 mice and mice with a blocked AKT pathway were more resistant to infection than wild type (WT) mice, with a significantly lower infection rate, longer survival time and less parasite load, as well as an increased secretion level of IL-12p40 and IFN-γ. Kinetoplastid membrane protein-11 (KMP-11) of TeEVs could activate AKT pathway and inhibit the productions of IL-12p40, TNF-α, and IL-6 . TeEVs and KMP-11 could inhibit the productions of IL-12p40 and IFN-γ, promote proliferation and shorten the survival time of infected mice . In conclusion, could escape host immune response through inhibiting the productions of inflammatory cytokines via secreting TeEVs to activate TLR2-AKT pathway. KMP-11 in TeEVs was involved in promoting infection.Extracellular vesicles (EVs) secreted by () activate the TLR2-AKT signaling pathway to inhibit the production of inflammatory cytokines, thereby escaping the host's immune response. Kinetoplastid membrane protein-11 (KMP-11) in EVs is related to the promotion of infection via AKT pathway.

摘要

苏拉病是亚洲和南美洲最重要的具有经济后果的动物疾病之一，由 引起。然而， 的免疫逃避机制尚未得到广泛研究。在本研究中，我们对 细胞外囊泡 (TeEVs) 进行了表征，并研究了 TeEVs 在 感染中的作用。结果表明， 和 TeEVs 可以激活 TLR2-AKT 途径，抑制小鼠 BMDMs 中 IL-12p40、IL-6 和 TNF-α 的分泌。TLR2 缺陷型小鼠和 AKT 途径被阻断的小鼠比野生型 (WT) 小鼠对 感染更具抵抗力，感染率更低、存活时间更长、寄生虫载量更低，同时 IL-12p40 和 IFN-γ 的分泌水平更高。TeEVs 中的金葡菌膜蛋白 11 (KMP-11) 可以激活 AKT 途径并抑制 IL-12p40、TNF-α 和 IL-6 的产生。TeEVs 和 KMP-11 可以抑制 IL-12p40 和 IFN-γ 的产生，促进 增殖，并缩短感染小鼠的存活时间。总之， 通过分泌 TeEVs 激活 TLR2-AKT 途径来抑制炎症细胞因子的产生，从而逃避宿主的免疫反应。TeEVs 中的 KMP-11 参与通过 AKT 途径促进 感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/1be3e6cfdee6/KVIR_A_1959495_F0010_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/5d071f974c86/KVIR_A_1959495_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/2f952bc960ce/KVIR_A_1959495_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/7b60a86fbbe5/KVIR_A_1959495_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/21f699d24ae3/KVIR_A_1959495_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/b3012a02eb0e/KVIR_A_1959495_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/0a6f248d8044/KVIR_A_1959495_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/53333e941d10/KVIR_A_1959495_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/eb7da3938b55/KVIR_A_1959495_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/1dbdabfa5163/KVIR_A_1959495_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/c2e399b14b99/KVIR_A_1959495_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/1be3e6cfdee6/KVIR_A_1959495_F0010_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/5d071f974c86/KVIR_A_1959495_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/2f952bc960ce/KVIR_A_1959495_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/7b60a86fbbe5/KVIR_A_1959495_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/21f699d24ae3/KVIR_A_1959495_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/b3012a02eb0e/KVIR_A_1959495_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/0a6f248d8044/KVIR_A_1959495_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/53333e941d10/KVIR_A_1959495_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/eb7da3938b55/KVIR_A_1959495_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/1dbdabfa5163/KVIR_A_1959495_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/c2e399b14b99/KVIR_A_1959495_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7aeb/8344757/1be3e6cfdee6/KVIR_A_1959495_F0010_OC.jpg

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