Modulation of macrophage efferocytosis in inflammation.
Modulation of macrophage efferocytosis in inflammation.
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DOI：
10.3389/fimmu.2011.00057
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发表时间：
2011
影响因子：
7.3
通讯作者：
Bratton DL
中科院分区：
文献类型：
--
作者：
Korns D;Frasch SC;Fernandez-Boyanapalli R;Henson PM;Bratton DL
巨噬细胞在炎症环境中的一项关键功能是通过一种特殊的吞噬过程来清除濒临死亡的细胞，这种吞噬过程被称为吞噬作用(“带入坟墓”)。吞噬巨噬细胞通过特异性受体结合和下游信号的诱导，通过以下方式促进炎症消退：(1)有效地吞噬死亡细胞，从而避免细胞破坏和炎症内容物的释放；(2)产生抗炎介质，如IL-10和转化生长因子-β，抑制促炎反应。有证据表明，巨噬细胞编程的可塑性，对不断变化的环境线索做出反应，调节泡泡细胞的能力。激活核受体PPARγ、PPARδ、LxR，可能还有RxRα是增强泡腾作用编程的关键。此外，炎症环境中的一些信号，包括那些来自死亡细胞本身的信号，可以通过作为即时抑制/增强剂或通过改变巨噬细胞编程以实现长期效果来影响泡腾细胞的效率。重要的是，巨噬细胞持续的炎性编程可导致缺陷的凋亡细胞清除，并与自身免疫和其他慢性炎症性疾病的发展有关。该综述总结了目前对调节巨噬细胞泡核能力的多种因素的认识，并重点介绍了在限制慢性炎症方面具有重要潜力的新的治疗靶点。
A critical function of macrophages within the inflammatory milieu is the removal of dying cells by a specialized phagocytic process called efferocytosis (“to carry to the grave”). Through specific receptor engagement and induction of downstream signaling, efferocytosing macrophages promote resolution of inflammation by (i) efficiently engulfing dying cells, thus avoiding cellular disruption and release of inflammatory contents, and (ii) producing anti-inflammatory mediators such as IL-10 and TGF-β that dampen pro-inflammatory responses. Evidence suggests that plasticity in macrophage programming, in response to changing environmental cues, modulates efferocytic capability. Essential to programming for enhanced efferocytosis is activation of the nuclear receptors PPARγ, PPARδ, LXR, and possibly RXRα. Additionally, a number of signals in the inflammatory milieu, including those from dying cells themselves, can influence efferocytic efficacy either by acting as immediate inhibitors/enhancers or by altering macrophage programming for longer-term effects. Importantly, sustained inflammatory programming of macrophages can lead to defective apoptotic cell clearance and is associated with development of autoimmunity and other chronic inflammatory disorders. This review summarizes the current knowledge of the multiple factors that modulate macrophage efferocytic ability and highlights emerging therapeutic targets with significant potential for limiting chronic inflammation.
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影响因子：
15.9
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM
DOI：
10.4049/jimmunol.1001778
发表时间：
2010-10-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Fernandez-Boyanapalli R;McPhillips KA;Frasch SC;Janssen WJ;Dinauer MC;Riches DW;Henson PM;Byrne A;Bratton DL
通讯作者：
Bratton DL
影响因子：
5.5
作者：
Banerjee, Sami;Friggeri, Arnaud;Abraham, Edward
通讯作者：
Abraham, Edward
影响因子：
16
作者：
Ghisletti, Serena;Huang, Wendy;Glass, Christopher K.
通讯作者：
Glass, Christopher K.
影响因子：
29
作者：
Bouhlel, M. Amine;Derudas, Bruno;Chinetti-Gbaguidi, Giulia
通讯作者：
Chinetti-Gbaguidi, Giulia