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胞内 ROS 通过 JAK/STAT 和 Toll 激活途径激活先天免疫系统。

Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation.

机构信息

Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India.

Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India.

出版信息

Cell Rep. 2020 Nov 10;33(6):108368. doi: 10.1016/j.celrep.2020.108368.

DOI:10.1016/j.celrep.2020.108368
PMID:33176146
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7662148/
Abstract

Tissue injury is one of the most severe environmental perturbations for a living organism. When damage occurs in adult Drosophila, there is a local response of the injured tissue and a coordinated action across different tissues to help the organism overcome the deleterious effect of an injury. We show a change in the transcriptome of hemocytes at the site of tissue injury, with pronounced activation of the Toll signaling pathway. We find that induction of the cytokine upd-3 and Toll receptor activation occur in response to injury alone, in the absence of a pathogen. Intracellular accumulation of hydrogen peroxide in hemocytes is essential for upd-3 induction and is facilitated by the diffusion of hydrogen peroxide through a channel protein Prip. Importantly, hemocyte activation and production of reactive oxygen species (ROS) at the site of a sterile injury provide protection to flies on subsequent infection, demonstrating training of the innate immune system.

摘要

组织损伤是生物体面临的最严重的环境干扰之一。在成年果蝇中,当组织受到损伤时,会有局部的反应,同时不同组织也会协调行动,帮助生物体克服损伤带来的有害影响。我们发现,组织损伤部位的血细胞转录组发生了变化,Toll 信号通路被显著激活。我们发现,细胞因子 upd-3 的诱导和 Toll 受体的激活仅在没有病原体的情况下,单独对损伤做出反应而发生。在血细胞中,过氧化氢的细胞内积累对于 upd-3 的诱导是必不可少的,而过氧化氢通过通道蛋白 Prip 的扩散促进了这种积累。重要的是,在无菌损伤部位,血细胞的激活和活性氧(ROS)的产生为随后的感染提供了对果蝇的保护,这表明先天免疫系统得到了训练。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/b6214fbc69ca/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/7d3bd5a36fc4/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/ad3ac603f3ac/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/df977dc40b66/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/edf3ba6f77cb/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/64aa51366ceb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/35a55afe2e5c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/b6214fbc69ca/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/7d3bd5a36fc4/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/ad3ac603f3ac/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/df977dc40b66/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/edf3ba6f77cb/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/64aa51366ceb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/35a55afe2e5c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/384c/7662148/b6214fbc69ca/gr6.jpg

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