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A类巨噬细胞清道夫受体可减弱无菌性腹膜炎中CXC趋化因子的产生及中性粒细胞的早期浸润。

The class A macrophage scavenger receptor attenuates CXC chemokine production and the early infiltration of neutrophils in sterile peritonitis.

作者信息

Cotena Alessia, Gordon Siamon, Platt Nick

机构信息

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3QX, UK.

出版信息

J Immunol. 2004 Nov 15;173(10):6427-32. doi: 10.4049/jimmunol.173.10.6427.

Abstract

The macrophage scavenger receptor (SR-A) is a multifunctional receptor that is associated with several important pathological conditions, including atherosclerosis. In this study, we show, using a sterile peritonitis model, that it can regulate the inflammatory response. SR-A null mice display an increased initial granulocytic infiltration because of overproduction of the CXC chemokines, MIP-2 and keratinocyte-derived cytokine. This differential response is dependent upon particle internalization and can be mimicked by advanced glycation end product-BSA-conjugated latex beads. Thus SR-A is a nonactivating receptor, which is the first example of a pattern recognition receptor that serves to counter the activities of proinflammatory receptors and attenuates the production of specific chemokines to ensure an inflammatory response of the appropriate magnitude.

摘要

巨噬细胞清道夫受体(SR-A)是一种多功能受体,与包括动脉粥样硬化在内的多种重要病理状况相关。在本研究中,我们利用无菌性腹膜炎模型表明,它可调节炎症反应。SR-A基因敲除小鼠由于CXC趋化因子、巨噬细胞炎症蛋白-2(MIP-2)和角质形成细胞衍生细胞因子的过度产生,初始粒细胞浸润增加。这种差异反应依赖于颗粒内化,并且可被晚期糖基化终产物-牛血清白蛋白缀合乳胶珠模拟。因此,SR-A是一种非激活受体,这是模式识别受体的首个实例,其作用是对抗促炎受体的活性并减弱特定趋化因子的产生,以确保适度的炎症反应。

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