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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Endogenous ligands of Toll-like receptors
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Endogenous ligands of Toll-like receptors

机译：Toll样受体的内源性配体

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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(s) 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(s) 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(s), before exploring further the implication and therapeutic potential of these putative TLR ligands.
机译：大量的工作表明，许多内源性分子，例如热休克蛋白（hsp），可能是先天免疫系统的有效激活剂，能够诱导单核巨噬细胞系统促炎性细胞因子的产生以及树突状细胞的激活和成熟。这些内源性分子的细胞因子样作用是通过Toll样受体（TLR）信号转导途径介导的，其方式类似于脂多糖（LPS;通过TLR4）和细菌脂蛋白（通过TLR2）。但是，最近的证据表明，所报道的hsp的细胞因子效应可能是LPS和LPS相关分子污染的结果。先前无法识别造成hsp假定的TLR配体的污染物的原因包括未能使用不含LPS污染的高度纯化的hsp;无法识别LPS的热敏感性;并且没有考虑除LPS以外的其他污染物。尚不清楚其他报道的TLR2和TLR4推定的内源性配体是否是与病原体相关的分子模式污染的结果。在进一步探索这些推定的TLR配体的含义和治疗潜力之前，必须努力确定所有报告的TLR推定的内源性配体是内源性分子还是污染物的结果。

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