The sterile inflammatory response.
The sterile inflammatory response.
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DOI：
10.1146/annurev-immunol-030409-101311
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发表时间：
2010
影响因子：
29.7
通讯作者：
Kono H
中科院分区：
文献类型：
--
作者：
Rock KL;Latz E;Ontiveros F;Kono H
急性炎症反应是一把双刃剑。一方面，它在最初的宿主防御中起着关键作用，特别是对许多感染。另一方面，它的目标是不精确的，因此，当它被卷入战斗时，它可能会对组织造成附带损害。在刺激是无菌的情况下，成本效益比可能很高;正因为如此，无菌炎症是许多疾病的发病机制的基础。虽然我们对微生物如何引发炎症的理解已经取得了重大进展，但在无菌情况下对这一过程的了解要少得多。这篇综述集中在一个子集的许多无菌刺激，可以诱导炎症-特别是死细胞和各种刺激性颗粒，包括晶体，矿物质和蛋白质聚集体。虽然这一刺激子集在结构上非常多样化，并且可能看起来不相关，但越来越多的证据表明，先天免疫系统可能以类似的方式识别它们，并通过共同的途径刺激无菌炎症反应。在这里，我们回顾了关于这些反应的已有和新出现的数据。
The acute inflammatory response is a double-edged sword. On the one hand it plays a key role in initial host defense particularly against many infections. On the other hand its aim is imprecise and as a consequence, when it is drawn into battle, it can cause collateral damage in tissues. In situations where the inciting stimulus is sterile, the cost-benefit ratio may be high; because of this, sterile inflammation underlies the pathogenesis of a number of diseases. While there have been major advances in our understanding of how microbes trigger inflammation, much less has been learned about this process in sterile situations. This review focuses on a subset of the many sterile stimuli that can induce inflammation – specifically dead cells and a variety of irritant particles, including crystals, minerals, and protein aggregates. Although this subset of stimuli is structurally very diverse and might appear to be unrelated, there is accumulating evidence that the innate immune system may recognize them in similar ways and stimulate the sterile inflammatory response via common pathways. Here we review established and emerging data about these responses.
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影响因子：
82.9
作者：
Chen, Chun-Jen;Kono, Hajime;Rock, Kenneth L.
通讯作者：
Rock, Kenneth L.
影响因子：
30.5
作者：
Buerckstuemmer, Tilmann;Baumann, Christoph;Superti-Furga, Giulio
通讯作者：
Superti-Furga, Giulio
影响因子：
5.5
作者：
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通讯作者：
Hamilton, TA
影响因子：
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作者：
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通讯作者：
Liles, W. Conrad
影响因子：
6.3
作者：
Abulafia, Denise P.;Vaccari, Juan Pablo de Rivero;Dietrich, W. Dalton
通讯作者：
Dietrich, W. Dalton