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Notch信号通路在健康与疾病中调节固有免疫和炎症反应中的作用。

Role of Notch signaling in regulating innate immunity and inflammation in health and disease.

作者信息

Shang Yingli, Smith Sinead, Hu Xiaoyu

机构信息

School of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China.

Department of Clinical Medicine, Trinity College Dublin, Dublin, 2, Ireland.

出版信息

Protein Cell. 2016 Mar;7(3):159-74. doi: 10.1007/s13238-016-0250-0. Epub 2016 Mar 2.

DOI:10.1007/s13238-016-0250-0
PMID:26936847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4791423/
Abstract

The Notch signaling pathway is conserved from Drosophila to mammals and is critically involved in developmental processes. In the immune system, it has been established that Notch signaling regulates multiple steps of T and B cell development in both central and peripheral lymphoid organs. Relative to the well documented role of Notch signaling in lymphocyte development, less is known about its role in regulating myeloid lineage development and function, especially in the context of acute and chronic inflammation. In this review article, we will describe the evidence accumulated during the recent years to support a key regulatory role of the Notch pathway in innate immune and inflammatory responses and discuss the potential implications of such regulation for pathogenesis and therapy of inflammatory disorders.

摘要

Notch信号通路从果蝇到哺乳动物都是保守的,并且在发育过程中起着关键作用。在免疫系统中,已经确定Notch信号通路调节中枢和外周淋巴器官中T细胞和B细胞发育的多个步骤。相对于Notch信号通路在淋巴细胞发育中已被充分记录的作用,人们对其在调节髓系谱系发育和功能方面的作用了解较少,尤其是在急性和慢性炎症的背景下。在这篇综述文章中,我们将描述近年来积累的证据,以支持Notch通路在先天免疫和炎症反应中的关键调节作用,并讨论这种调节对炎症性疾病发病机制和治疗的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/31b02a2d5841/13238_2016_250_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/a98bf96f8c92/13238_2016_250_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/5cb387743d0c/13238_2016_250_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/31b02a2d5841/13238_2016_250_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/a98bf96f8c92/13238_2016_250_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/5cb387743d0c/13238_2016_250_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3858/4791423/31b02a2d5841/13238_2016_250_Fig3_HTML.jpg

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NOTCH reprograms mitochondrial metabolism for proinflammatory macrophage activation.NOTCH通过重编程线粒体代谢来激活促炎巨噬细胞。
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Osteopetrosis in TAK1-deficient mice owing to defective NF-κB and NOTCH signaling.由于NF-κB和NOTCH信号通路缺陷,TAK1基因敲除小鼠出现骨质硬化症。
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