Can phage display be used as a tool to functionally identify endogenous eat-me signals in phagocytosis?
Can phage display be used as a tool to functionally identify endogenous eat-me signals in phagocytosis?
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DOI：
10.1177/1087057109335679
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发表时间：
2009-07
影响因子：
--
通讯作者：
Li W
中科院分区：
文献类型：
--
作者：
Caberoy NB;Zhou Y;Li W
通过吞噬作用清除凋亡细胞和细胞碎片对发育、组织稳态和炎症的解决至关重要。Eat-me信号控制吞噬的开始，这是我们理解吞噬细胞生物学的关键。由于缺乏功能性克隆策略，吃我信号通常是在个案的基础上识别和表征的。为了研究通过噬菌体展示功能克隆eat-me信号的可行性，我们对T7噬菌体显示两种众所周知的eat-me信号的生物学行为进行了表征：生长抑制特异性基因6 （Gas6）和乳脂球egf8 （MFG-E8）。Gas6噬菌体结合所有三种已知的Gas6受体，Mer， Axl和Tyro3受体酪氨酸激酶。gas6噬菌体和mfg - e8噬菌体能够与吞噬细胞和非吞噬细胞结合。然而，这两种噬菌体仅在吞噬细胞中刺激噬菌体摄取，包括巨噬细胞、小胶质细胞和视网膜色素上皮（RPE）细胞，而在非吞噬细胞中没有。此外，吞噬细胞中吞噬选择的功能噬菌体丰富了gas6噬菌体和mfg - e8噬菌体，这表明噬菌体展示可以作为一种工具，从噬菌体展示cDNA文库中功能鉴定未知的吞噬信号。
Removal of apoptotic cells and cellular debris by phagocytosis is essential for development, tissue homeostasis and resolution of inflammation. Eat-me signals control the initiation of phagocytosis, holding a key to our understanding of phagocyte biology. Due to lack of functional cloning strategy, eat-me signals are conventionally identified and characterized on a case-by-case basis. To investigate the feasibility of functionally cloning eat-me signals by phage display, we characterize the biological behavior of T7 phages displaying two well-known eat-me signals: growth arrest-specific gene 6 (Gas6) and milk fat globule-EGF8 (MFG-E8). Gas6-phage binds to all three known Gas6 receptors, Mer, Axl and Tyro3 receptor tyrosine kinases. Gas6-phage and MFG-E8-phage are capable of binding to phagocytes and non-phagocytes. However, both phages stimulate phage uptake only in phagocytes, including macrophages, microglia and retinal pigment epithelium (RPE) cells, but not in non-phagocytes. Furthermore, functional phage selection by phagocytosis in phagocytes enriches both Gas6-phage and MFG-E8-phage, suggesting that phage display can be used as a tool to functionally identify unknown eat-me signals from phage display cDNA library.
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影响因子：
5.3
作者：
MANFIOLETTI, G;BRANCOLINI, C;SCHNEIDER, C
通讯作者：
SCHNEIDER, C
影响因子：
4.2
作者：
D'Andrea, MR;Cole, GM;Ard, MD
通讯作者：
Ard, MD
影响因子：
30.8
作者：
Gal, A;Li, Y;Vollrath, D
通讯作者：
Vollrath, D
影响因子：
64.8
作者：
Park, Daeho;Tosello-Trampont, Annie-Carole;Ravichandran, Kodi S.
通讯作者：
Ravichandran, Kodi S.
影响因子：
3.5
作者：
D'Cruz, PM;Yasumura, D;Vollrath, D
通讯作者：
Vollrath, D