"Eat me" and "don't eat me" signals govern the innate immune response and tissue repair in the CNS: emphasis on the critical role of the complement system
"Eat me" and "don't eat me" signals govern the innate immune response and tissue repair in the CNS: emphasis on the critical role of the complement system
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DOI：
10.1016/s0161-5890(03)00109-3
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发表时间：
2003-09-01
影响因子：
3.6
通讯作者：
Gasque, P
中科院分区：
文献类型：
--
作者：
Elward, K;Gasque, P
完整的先天性免疫系统（例如补体系统、清道夫受体、Toll样受体（TLR））已在CNS中描述，并且被认为是设计用于对抗入侵病原体和毒性细胞碎片（例如凋亡细胞和淀粉样纤维）的极其有效的军队。可溶性或分泌的先天免疫分子与病原体相关分子模式（PAMP）以及凋亡细胞相关分子模式（ACAMP）的结合提供了几种“吃我”信号，以促进专业和业余吞噬细胞对入侵者的安全处置。这些模式由受体（模式识别受体，PRR;例如CR 3）解码，所述受体根据这些信号的含义控制吞噬作用和相关的炎症反应。重要的是，为了避免周围细胞的过度附带损伤，越来越明显的是，“不要吃我”信号（本文中称为自相关分子模式，SAMP;例如补体调节蛋白，CD 200）对于发出稳健的抗炎反应信号和促进组织修复是至关重要的。进一步了解CNS中的先天免疫应答将极大地有助于描绘新的治疗途径以保护免受CNS炎症和神经变性。(C)2003 Elsevier Ltd.保留所有权利。
A full innate immune system (e.g. complement system, scavenger receptors, Toll-like receptors (TLR)) has been described in the CNS and is thought to be an extremely efficient army designed to fight against invading pathogens and toxic cell debris such as apoptotic cells and amyloid fibrils. The binding of soluble or secreted innate immune molecules on pathogen-associated molecular patterns (PAMPs) as well as apoptotic cell-associated molecular patterns (ACAMPs) provide several "eat me" signals to promote the safe disposal of the intruders by professional and amateur phagocytes. These patterns are deciphered by receptors (pattern recognition receptors, PRRs; e.g. CR3) that control phagocytosis and associated inflammatory response depending on the meaning of these signals. Importantly, in order to avoid excessive collateral damage of surrounding cells, it is increasingly evident that "don't eat me" signals (coined herein as self-associated molecular patterns, SAMPs; e.g. complement regulatory proteins, CD200) are of paramount importance to signal a robust anti-inflammatory response and promote tissue repair. Further knowledge of the innate immune response in the CNS will greatly help to delineate the novel therapeutic routes to protect from CNS inflammation and neurodegeneration. (C) 2003 Elsevier Ltd. All rights reserved.