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Drosophila Relish‐mediated miR‐317 expression facilitates immune homeostasis restoration via inhibiting PGRP‐LC

机译:果蝇津津乐介导的 miR-317 表达通过抑制 PGRP-LC 促进免疫稳态恢复

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Abstract Innate immunity is the first and essential line for resisting pathogens, and the immune intensity and duration need to be strictly regulated to balance excessive or insufficient immune response. MicroRNAs (miRNAs) are crucial regulators of immune response in Drosophila, yet how immune‐related miRNAs are regulated remains poorly understood. Herein, we elucidated that the involvement of miR‐317 in NF‐κB transcription factor Relish mediated Drosophila Imd pathway in response to Gram‐negative (G‐) bacteria stimulation. Remarkably, the dynamic expression profiling for immune response indicated that Relish simultaneously enhances the expression of the effector antimicrobial peptide Dpt as well as miR‐317 post‐infection. Upregulation of miR‐317 could further down‐regulate the expression of PGRP‐LC, thereby forming a feedback in Drosophila Imd pathway to prevent over‐activation and restore immune homeostasis. Taken together, our study not only uncovers a novel Relish/miR‐317/PGRP‐LC regulatory axis to attenuate Drosophila Imd immune response and facilitate immune homeostasis restoration, but also provides vital insights into the complex mechanisms of animal innate immune regulation.
机译:抽象的先天免疫是第一步,基本线抵抗病原体,免疫需要严格的强度和持续时间调节平衡过多或不足免疫反应。监管机构在果蝇的免疫反应免疫相关的microrna应承担监管仍然是如何知之甚少。miR量317参与NFκB转录喜欢介导因素果蝇Imd通路应对克- (G)应承担的细菌刺激。分析表明,免疫反应喜欢的同时增强了表达效应抗菌肽Dpt以及米尔317岗位应承担的感染。可能会进一步下降量调节的表达吗PGRP应承担的LC,从而形成一个反馈在果蝇Imd通路的激活和预防恢复免疫内稳态。研究不仅揭示了小说喜欢/米尔317 / PGRP LC应承担监管轴减弱果蝇和Imd的免疫应答促进免疫内稳态恢复,但是还提供了重要的见解动物先天免疫机制的监管。

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