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冷休克 Y 框蛋白-1 在炎症、动脉粥样硬化和器官移植排斥反应中的作用。

Role of cold shock Y-box protein-1 in inflammation, atherosclerosis and organ transplant rejection.

机构信息

Department of Nephrology and Clinical Immunology, University Hospital RWTH-Aachen, Pauwelsstrasse 30, 52057 Aachen, Germany.

出版信息

Eur J Cell Biol. 2012 Jun-Jul;91(6-7):567-75. doi: 10.1016/j.ejcb.2011.07.001. Epub 2011 Sep 22.

DOI:10.1016/j.ejcb.2011.07.001
PMID:21943779
Abstract

Chemokines (chemoattractant cytokines) are crucial regulators of immune cell extravasation from the bloodstream into inflamed tissue. Dysfunctional regulation and perpetuated chemokine gene expression are linked to progressive chronic inflammatory diseases and, in respect to transplanted organs, may trigger graft rejection. RANTES (regulated upon activation, normal T cell expressed and secreted (also known as CCL5)) is a model chemokine with relevance in numerous inflammatory diseases where the innate immune response predominates. Transcription factor Y-box binding protein-1 (YB-1) serves as a trans-regulator of CCL5 gene transcription in vascular smooth muscle cells and leucocytes. This review provides an update on YB-1 as a mediator of inflammatory processes and focuses on the role of YB-1 in CCL5 expression in diseases with monocytic cell infiltrates, albeit acute or chronic. Paradigms of such diseases encompass atherosclerosis and transplant rejection where cold shock protein YB-1 takes a dominant role in transcriptional regulation.

摘要

趋化因子(趋化因子细胞因子)是免疫细胞从血液渗出到炎症组织的关键调节因子。功能失调的调节和持续的趋化因子基因表达与进行性慢性炎症性疾病有关,就移植器官而言,可能引发移植物排斥反应。RANTES(激活后调节、正常 T 细胞表达和分泌(也称为 CCL5))是一种模型趋化因子,在许多以先天免疫反应为主的炎症性疾病中具有相关性。转录因子 Y 框结合蛋白-1(YB-1)作为血管平滑肌细胞和白细胞中 CCL5 基因转录的反式调节剂。本文综述了 YB-1 作为炎症过程的介质,并重点介绍了 YB-1 在单核细胞浸润性疾病中 CCL5 表达中的作用,尽管这些疾病是急性或慢性的。此类疾病的范例包括动脉粥样硬化和移植排斥反应,其中冷休克蛋白 YB-1 在转录调控中发挥主导作用。

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