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树突状细胞中的核受体信号传导将脂质、基因组与免疫功能联系起来。

Nuclear receptor signalling in dendritic cells connects lipids, the genome and immune function.

作者信息

Szatmari Istvan, Nagy Laszlo

机构信息

Department of Biochemistry and Molecular Biology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.

出版信息

EMBO J. 2008 Sep 17;27(18):2353-62. doi: 10.1038/emboj.2008.160. Epub 2008 Aug 21.

DOI:10.1038/emboj.2008.160
PMID:18716631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2525841/
Abstract

Dendritic cells (DCs) are sentinels of the immune system and represent a heterogeneous cell population. The existence of distinct DC subsets is due to their inherent plasticity and to the changing microenvironment modulating their immunological properties. Numerous signalling pathways have impacts on DCs. It appears that besides cytokines/chemokines, lipid mediators also have profound effects on the immunogenicity of DCs. Some of these lipid mediators exert an effect through nuclear hormone receptors. Interestingly, more recent findings suggest that DCs are able to convert precursors to active hormones, ligands for nuclear receptors. Some of these DC-derived lipids, in particular retinoic acid (RA), have a central function in shaping T-cell development and effector functions. In this review, we summarize and highlight the function of a set of nuclear receptors (PPARgamma, RA receptor, vitamin D receptor and glucocorticoid receptor) in DC biology. Defining the contribution of nuclear hormone receptor signalling in DCs can help one to understand the regulatory logic of lipid signalling and allow the exploitation of their potential for therapeutic intervention in various immunological diseases.

摘要

树突状细胞(DCs)是免疫系统的哨兵,代表着异质性细胞群体。不同DC亚群的存在归因于其固有的可塑性以及调节其免疫特性的不断变化的微环境。众多信号通路对DCs有影响。除细胞因子/趋化因子外,脂质介质似乎也对DCs的免疫原性有深远影响。其中一些脂质介质通过核激素受体发挥作用。有趣的是,最近的研究结果表明,DCs能够将前体转化为活性激素,即核受体的配体。这些DC衍生的脂质中,特别是视黄酸(RA),在塑造T细胞发育和效应功能方面具有核心作用。在本综述中,我们总结并强调了一组核受体(过氧化物酶体增殖物激活受体γ、视黄酸受体、维生素D受体和糖皮质激素受体)在DC生物学中的功能。明确核激素受体信号在DCs中的作用有助于人们理解脂质信号的调节逻辑,并利用其潜力对各种免疫疾病进行治疗干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/8a148657ef09/emboj2008160f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/547736dc196a/emboj2008160f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/c333d7ed0bd5/emboj2008160f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/ccf002f04090/emboj2008160f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/8a148657ef09/emboj2008160f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/547736dc196a/emboj2008160f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/c333d7ed0bd5/emboj2008160f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/ccf002f04090/emboj2008160f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e23/2543048/8a148657ef09/emboj2008160f4.jpg

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