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抑制吞噬作用:生理学和疾病中的“别吃我”信号。

Putting the brakes on phagocytosis: "don't-eat-me" signaling in physiology and disease.

机构信息

Center for Cell Clearance, University of Virginia, Charlottesville, VA, USA.

Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA, USA.

出版信息

EMBO Rep. 2021 Jun 4;22(6):e52564. doi: 10.15252/embr.202152564. Epub 2021 May 27.

DOI:10.15252/embr.202152564
PMID:34041845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8183410/
Abstract

Timely removal of dying or pathogenic cells by phagocytes is essential to maintaining host homeostasis. Phagocytes execute the clearance process with high fidelity while sparing healthy neighboring cells, and this process is at least partially regulated by the balance of "eat-me" and "don't-eat-me" signals expressed on the surface of host cells. Upon contact, eat-me signals activate "pro-phagocytic" receptors expressed on the phagocyte membrane and signal to promote phagocytosis. Conversely, don't-eat-me signals engage "anti-phagocytic" receptors to suppress phagocytosis. We review the current knowledge of don't-eat-me signaling in normal physiology and disease contexts where aberrant don't-eat-me signaling contributes to pathology.

摘要

吞噬细胞及时清除死亡或病源细胞对于维持宿主内环境稳态至关重要。吞噬细胞在清除过程中具有高度的保真度,同时避免清除健康的邻近细胞,这个过程至少部分受到宿主细胞表面“吃我”和“别吃我”信号的平衡调控。在接触时,“吃我”信号激活吞噬细胞膜上表达的“促吞噬”受体,并发出信号促进吞噬作用。相反,“别吃我”信号则与“抗吞噬”受体结合,抑制吞噬作用。我们综述了“别吃我”信号在正常生理和疾病环境中的最新知识,其中异常的“别吃我”信号导致了病理改变。

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Shp1 Loss Enhances Macrophage Effector Function and Promotes Anti-Tumor Immunity.Shp1 缺失增强了巨噬细胞的效应功能,并促进了抗肿瘤免疫。
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CD47 Ligation Repositions the Inhibitory Receptor SIRPA to Suppress Integrin Activation and Phagocytosis.CD47 配体将抑制性受体 SIRPA 重新定位以抑制整合素激活和吞噬作用。
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Upregulation of CD47 Is a Host Checkpoint Response to Pathogen Recognition.CD47 的上调是宿主对病原体识别的检查点反应。
mBio. 2020 Jun 23;11(3):e01293-20. doi: 10.1128/mBio.01293-20.
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Clonally expanding smooth muscle cells promote atherosclerosis by escaping efferocytosis and activating the complement cascade.克隆扩增的平滑肌细胞通过逃避噬作用并激活补体级联反应促进动脉粥样硬化。
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Activation of JUN in fibroblasts promotes pro-fibrotic programme and modulates protective immunity.成纤维细胞中 JUN 的激活促进了促纤维化程序,并调节了保护性免疫。
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