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无菌性炎症的分子决定因素。

Molecular determinants of sterile inflammation.

机构信息

Department of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo 173-8605, Japan.

Department of Internal Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo 173-8605, Japan.

出版信息

Curr Opin Immunol. 2014 Feb;26:147-56. doi: 10.1016/j.coi.2013.12.004. Epub 2014 Jan 7.

Abstract

Necrotic cell death alerts the acquired immune system to activate naïve T cells even in the absence of non-self derived molecules (e.g. pathogens). In addition, sterile necrosis leads to innate immune-mediated acute inflammation. The dying cells still represent a threat to the body that should be eliminated by the host immune response. Although the inflammatory response plays important roles in protecting the host and repairing tissues, it can also cause the collateral damage to normal tissues that underlies disease pathogenesis. Tissue resident macrophages recognize the danger signals released from necrotic cells via the pattern recognition receptors and secrete IL-1 that results in acute neutrophilic inflammation. This article will review our current knowledge especially focusing on the role of IL-1 in the sterile necrotic cell death induced inflammation.

摘要

细胞坏死会向获得性免疫系统发出警报,即使没有非自身来源的分子(例如病原体),也能激活幼稚 T 细胞。此外,无菌性细胞坏死会导致固有免疫介导的急性炎症。垂死的细胞仍然对身体构成威胁,应该被宿主的免疫反应消除。尽管炎症反应在保护宿主和修复组织方面起着重要作用,但它也可能导致疾病发病机制所基于的正常组织的附带损伤。组织驻留巨噬细胞通过模式识别受体识别来自坏死细胞的危险信号,并分泌导致急性中性粒细胞炎症的白细胞介素 1。本文将综述我们目前的认识,特别是聚焦于白细胞介素 1 在无菌性细胞坏死诱导炎症中的作用。

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