Paying for the Tolls: The High Cost of the Innate Immune System for the Cardiac Myocyte.
Paying for the Tolls: The High Cost of the Innate Immune System for the Cardiac Myocyte.
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DOI：
10.1007/978-3-319-57613-8_2
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发表时间：
2017
影响因子：
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通讯作者：
A. Knowlton
中科院分区：
文献类型：
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作者：
A. Knowlton
心肌细胞与免疫系统的特化细胞有显著的不同，免疫系统对入侵生物和组织损伤有两种不同的反应。适应性或获得性免疫产生高度特异性的抗体以应对威胁，并且是免疫的重要组成部分;然而，适应性免疫可能需要4-7天才能动员，并且更原始的反应，先天免疫，填补了差距。先天免疫在复杂和原始的生命形式中表现出来。广泛分布于不同组织的特化受体Toll样受体（TLR）识别危险信号，并迅速响应释放有害物质，如TNFα。问题是，已经发现许多内源性分子作为特定TLR的配体，当这些分子释放到细胞外环境中时，它们可以通过激活先天免疫和炎症反应引起问题。在心肌细胞中，热休克蛋白（HSP）60可以激活TLR 4，HMGB 1也可以，这种类型的反应可以放大对缺血/再灌注的反应，导致细胞和组织损伤增加。TLR的激活可能潜在地放大慢性炎性疾病，例如缺血性心力衰竭。因此，了解TLR的调控及其下游效应是很重要的。本章将重点介绍TLR和心肌细胞。
The cardiac myocyte differs strikingly from the specialized cells of the immune system, which has two different responses to invading organisms and tissue damage. Adaptive or acquired immunity generates highly specific antibodies in response to threats and is an essential component of immunity; however, adaptive immunity can take 4–7 days to mobilize, and a more primitive response, innate immunity, fills the gap. Innate immunity is expressed in complex and in primitive life forms. Specialized receptors, Toll-like receptors (TLRs), which are widely distributed throughout different tissues recognize danger signals and rapidly respond with the release of noxious substances, such as TNFα. The problem is that many endogenous molecules have been found to act as ligands for specific TLRs, and when these molecules are released into the extracellular environment, they can cause problems by activating innate immunity and an inflammatory response. In cardiac myocytes heat shock protein (HSP)60 can activate TLR4, as can HMGB1, and this type of response can amplify the response to ischemia/reperfusion leading to increased cell and tissue injury. Activation of TLRs can potentially amplify chronic, inflammatory diseases, such as ischemic heart failure. Thus, it is important to understand the regulation of the TLRs and their downstream effects. This chapter will focus on the TLRs and cardiac myocytes.