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一种向免疫系统警示细胞死亡的危险信号的分子鉴定。

Molecular identification of a danger signal that alerts the immune system to dying cells.

作者信息

Shi Yan, Evans James E, Rock Kenneth L

机构信息

Department of Pathology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.

出版信息

Nature. 2003 Oct 2;425(6957):516-21. doi: 10.1038/nature01991. Epub 2003 Sep 7.

Abstract

In infections, microbial components provide signals that alert the immune system to danger and promote the generation of immunity. In the absence of such signals, there is often no immune response or tolerance may develop. This has led to the concept that the immune system responds only to antigens perceived to be associated with a dangerous situation such as infection. Danger signals are thought to act by stimulating dendritic cells to mature so that they can present foreign antigens and stimulate T lymphocytes. Dying mammalian cells have also been found to release danger signals of unknown identity. Here we show that uric acid is a principal endogenous danger signal released from injured cells. Uric acid stimulates dendritic cell maturation and, when co-injected with antigen in vivo, significantly enhances the generation of responses from CD8+ T cells. Eliminating uric acid in vivo inhibits the immune response to antigens associated with injured cells, but not to antigens presented by activated dendritic cells. Our findings provide a molecular link between cell injury and immunity and have important implications for vaccines, autoimmunity and inflammation.

摘要

在感染过程中,微生物成分会发出信号,提醒免疫系统存在危险并促进免疫反应的产生。如果没有这些信号,通常就不会有免疫反应,或者可能会形成免疫耐受。这就引出了这样一个概念,即免疫系统只对那些被认为与感染等危险情况相关的抗原做出反应。危险信号被认为是通过刺激树突状细胞成熟来发挥作用的,这样它们就能呈递外来抗原并刺激T淋巴细胞。人们还发现,濒死的哺乳动物细胞会释放身份不明的危险信号。在此我们表明,尿酸是受损细胞释放的主要内源性危险信号。尿酸会刺激树突状细胞成熟,并且在体内与抗原共同注射时,能显著增强CD8+ T细胞的反应。在体内消除尿酸会抑制对与受损细胞相关抗原的免疫反应,但不会抑制活化树突状细胞呈递抗原所引发的免疫反应。我们的研究结果在细胞损伤与免疫之间建立了分子联系,对疫苗、自身免疫和炎症具有重要意义。

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