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【Leukocyte Biology编译】
Min-Fu Tsan*, ,1 and Baochong Gao*,
* Research Service, VA Medical Center, Washington, DC;
Department of Medicine, Georgetown University, Washington, DC; and
Department of Medicine, George Washington University, Washington, DC
(Journal of Leukocyte Biology. 2004;76:514-519.)
© 2004
Extensive work has suggested that a number of endogenous molecules such as heat shock proteins (hsp) may be potent activators of the innate immune system capable of inducing proinflammatory cytokine production by the monocyte-macrophage system and the activation and maturation of dendritic cells. The cytokine-like effects of these endogenous molecules are mediated via the Toll-like receptor (TLR) signal-transduction pathways in a manner similar to lipopolysaccharide (LPS; via TLR4) and bacterial lipoproteins (via TLR2). However, recent evidence suggests that the reported cytokine effects of hsp may be a result of the contaminating LPS and LPS-associated molecules. The reasons for previous failure to recognize the contaminant being responsible for the putative TLR ligands of hsp include failure to use highly purified hsp free of LPS contamination; failure to recognize the heat sensitivity of LPS; and failure to consider contaminant other than LPS. Whether other reported putative endogenous ligands of TLR2 and TLR4 are a result of contamination of pathogen-associated molecular patterns is not clear. It is essential that efforts should be directed to conclusively determine whether the reported putative endogenous ligands of TLRs are a result of the endogenous molecules or of contaminant, before exploring further the implication and therapeutic potential of these putative TLR ligands.
众多的研究工作证实有很多的像热休克蛋白等内源性分子可能是固有免疫系统的强大激活剂,能够诱导单核-巨噬系统和活化、成熟的树突状细胞分泌前炎症细胞因子.这些内源性分子的细胞因子样效应是通过Toll-like 受体(TLR) 信号转道途径,其作用方式类似脂多糖(LPS,经过TLR4途径)以及细菌的脂蛋白(经TLR2途径).然而,近来的研究证据表明以前报道的这些热休克蛋白的细胞因子样效应可能是污染了脂多糖或脂多糖相关分子.而在以前没有认识这种污染主要由于其公认的热休克蛋白的TLR配体:包括没有能够用高纯度的无LPS的HSP;没有认识到脂多糖的热敏感性以及没有把LPS看作为污染.尽管那些报道的推断内源性配体TLR2,TLR4是病原体相关污染的结果还不清楚,但在进一步探讨起相关的潜在的治疗作用有必要努力最终确定这种假定的内源性配体TLR到底是内源性分子还是污染的结果.
Endogenous ligands of Toll-like receptors
Min-Fu Tsan*, ,1 and Baochong Gao*,
* Research Service, VA Medical Center, Washington, DC;
Department of Medicine, Georgetown University, Washington, DC; and
Department of Medicine, George Washington University, Washington, DC
(Journal of Leukocyte Biology. 2004;76:514-519.)
© 2004 有全文吗？谢谢：suyy511@sina.com 附上全文，谨供参考
514.pdf (80.79k) Active participation of endothelial cells in inflammation
Joan M. Cook-Mills @ and Tracy L. Deem
Department of Pathology and Laboratory Medicine, University of Cincinnati, Ohio
@ To whom correspondence should be addressed. E-mail: joan.cook@uc.edu.
Published online before print January 3, 2005
This Article
© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0904554
Received for publication September 29, 2004.
Revised October 15, 2004.
Accepted for publication December 7, 2004.
Abstract
Leukocyte migration from the blood into tissues is vital for immune surveillance and inflammation. During this diapedesis of leukocytes, the leukocytes bind to endothelial cell adhesion molecules and then migrate across the vascular endothelium. Endothelial cell adhesion molecules and their counter-receptors on leukocytes generate intracellular signals. This review focuses on the active function of endothelial cells during leukocyte-endothelial cell interactions. We include a discussion of the "outside-in" signals in endothelial cells, which are stimulated by antibody cross-linking or leukocyte binding to platelet-endothelial cell adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1. Some of these signals in endothelial cells have been demonstrated to actively participate in leukocyte migration. We suggest that some of the adhesion molecule signals, which have not been assigned a function, are consistent with signals that stimulate retraction of lateral junctions, stimulate endothelial cell basal surface adhesion, or induce gene expression
炎症中内皮细胞的活跃功能
白细胞的从血液到组织的迁移是机体免疫监视和炎症反应中起着至关重要的功能。在白细胞的渗出过程中，白细胞结合到内皮细胞黏附分子并通过血管内皮，内皮细胞黏附分子与其在白细胞上的相应受体结合产生胞内信号。本宗述集中讨论白-内皮细胞相互作用中内皮细胞的活跃功能以及由抗体胶连或白细胞与血小板-内皮细胞黏附分子-1（ECAM-I）、胞间黏附分子-1（IAM-1）、血管细胞黏附分子-1（VCAM-1）结合所刺激产生的内皮细胞“内-外”信号。其中的一些信号已经证明积极参与白细胞的迁移。我们认为其中的一些黏附分子信号不光是起某种单一的功能，而是与那些刺激细胞间连接收缩、内皮细胞基底黏附以及诱导基因表达等的信号一起协调起作用。
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作者:admin@医学,生命科学 2011-06-11 17:30
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