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The specific recognition by macrophages of CD8+,CD45RO+ T cells undergoing apoptosis: a mechanism for T cell clearance during resolution of viral infections.巨噬细胞对正在经历凋亡的CD8⁺、CD45RO⁺ T细胞的特异性识别：病毒感染消退过程中T细胞清除的一种机制。
J Exp Med. 1994 Nov 1;180(5):1943-7. doi: 10.1084/jem.180.5.1943.
2
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Effector cells derived from host CD8 memory T cells mediate rapid resistance against minor histocompatibility antigen-mismatched allogeneic marrow grafts without participation of perforin, Fas ligand, and the simultaneous inhibition of 3 tumor necrosis factor family effector pathways.源自宿主CD8记忆T细胞的效应细胞介导对次要组织相容性抗原错配的同种异体骨髓移植的快速抗性，且无需穿孔素、Fas配体参与，同时抑制3种肿瘤坏死因子家族效应途径。
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Homeostatic regulation of CD8+ T cells by perforin.穿孔素对CD8 + T细胞的稳态调节
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Perforin-independent CD8(+) T-cell-mediated cytotoxicity of alveolar epithelial cells is preferentially mediated by tumor necrosis factor-alpha: relative insensitivity to Fas ligand.穿孔素非依赖性CD8(+) T细胞介导的肺泡上皮细胞细胞毒性主要由肿瘤坏死因子-α介导：对Fas配体相对不敏感。
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The significance of low bcl-2 expression by CD45RO T cells in normal individuals and patients with acute viral infections. The role of apoptosis in T cell memory.正常个体及急性病毒感染患者中CD45RO T细胞低bcl-2表达的意义。细胞凋亡在T细胞记忆中的作用。
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Single-cell perforin and granzyme expression reveals the anatomical localization of effector CD8+ T cells in influenza virus-infected mice.单细胞穿孔素和颗粒酶表达揭示了流感病毒感染小鼠中效应性CD8 + T细胞的解剖定位。
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Human glomerular mesangial cell phagocytosis of apoptotic neutrophils: mediation by a novel CD36-independent vitronectin receptor/thrombospondin recognition mechanism that is uncoupled from chemokine secretion.人肾小球系膜细胞对凋亡中性粒细胞的吞噬作用：由一种新的不依赖CD36的玻连蛋白受体/血小板反应蛋白识别机制介导，该机制与趋化因子分泌无关。
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Monocytes recruited to the lungs of mice during immune inflammation ingest apoptotic cells poorly.在免疫炎症期间招募到小鼠肺部的单核细胞吞噬凋亡细胞的能力较差。
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Reconstitution of CD4+ T cell responses in HIV-1 infected individuals initiating highly active antiretroviral therapy (HAART) is associated with renewed interleukin-2 production and responsiveness.开始接受高效抗逆转录病毒疗法（HAART）的HIV-1感染者中，CD4 + T细胞反应的重建与白细胞介素-2的重新产生和反应性有关。
Clin Exp Immunol. 2003 Oct;134(1):98-106. doi: 10.1046/j.1365-2249.2003.02256.x.
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Activation of protein kinase C beta II by the stereo-specific phosphatidylserine receptor is required for phagocytosis of apoptotic thymocytes by resident murine tissue macrophages.驻留小鼠组织巨噬细胞对凋亡胸腺细胞的吞噬作用需要立体特异性磷脂酰丝氨酸受体激活蛋白激酶CβII。
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Recognition and phagocytosis of apoptotic T cells by resident murine tissue macrophages require multiple signal transduction events.驻留的小鼠组织巨噬细胞对凋亡T细胞的识别和吞噬作用需要多个信号转导事件。
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Deficient in vitro and in vivo phagocytosis of apoptotic T cells by resident murine alveolar macrophages.驻留的小鼠肺泡巨噬细胞对凋亡T细胞的体外和体内吞噬作用不足。
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Antiinflammatory effects of CD95 ligand (FasL)-induced apoptosis.CD95配体（FasL）诱导的细胞凋亡的抗炎作用。
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本文引用的文献

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Phagocyte recognition of cells undergoing apoptosis.吞噬细胞对正在经历凋亡的细胞的识别。
Immunol Today. 1993 Mar;14(3):131-6. doi: 10.1016/0167-5699(93)90215-7.
2
The significance of low bcl-2 expression by CD45RO T cells in normal individuals and patients with acute viral infections. The role of apoptosis in T cell memory.正常个体及急性病毒感染患者中CD45RO T细胞低bcl-2表达的意义。细胞凋亡在T细胞记忆中的作用。
J Exp Med. 1993 Aug 1;178(2):427-38. doi: 10.1084/jem.178.2.427.
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The progressive differentiation of primed T cells is associated with an increasing susceptibility to apoptosis.已致敏T细胞的渐进分化与细胞凋亡易感性增加有关。
Eur J Immunol. 1994 Apr;24(4):892-9. doi: 10.1002/eji.1830240417.
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Immune exhaustion: driving virus-specific CD8+ T cells to death.免疫耗竭：促使病毒特异性CD8 + T细胞走向死亡。
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bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages.bcl-2抑制中性粒细胞的凋亡，但不抑制巨噬细胞对它们的吞噬作用。
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Long-term T-cell-mediated immunity to Epstein-Barr virus.针对爱泼斯坦-巴尔病毒的长期T细胞介导免疫
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7
Isolation and biochemical and functional characterization of perforin 1 from cytolytic T-cell granules.从细胞毒性T细胞颗粒中分离穿孔素1并进行生化及功能特性分析。
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Monoclonal antibodies detecting discrete epitopes of human perforin.
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9
Expression of CD45R0 (UCHL1) by CD4+ and CD8+ T cells as a sign of in vivo activation in infectious mononucleosis.CD4⁺和CD8⁺T细胞表达CD45R0（UCHL1）作为传染性单核细胞增多症体内活化的标志。
Clin Exp Immunol. 1991 Mar;83(3):447-51. doi: 10.1111/j.1365-2249.1991.tb05659.x.
10
Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.凋亡淋巴细胞表面磷脂酰丝氨酸的暴露会引发巨噬细胞的特异性识别与清除。
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巨噬细胞对正在经历凋亡的CD8⁺、CD45RO⁺ T细胞的特异性识别：病毒感染消退过程中T细胞清除的一种机制。

The specific recognition by macrophages of CD8+,CD45RO+ T cells undergoing apoptosis: a mechanism for T cell clearance during resolution of viral infections.

作者信息

Akbar A N, Savill J, Gombert W, Bofill M, Borthwick N J, Whitelaw F, Grundy J, Janossy G, Salmon M

机构信息

Department of Clinical Immunology, Royal Free Hospital School of Medicine, London, United Kingdom.

出版信息

J Exp Med. 1994 Nov 1;180(5):1943-7. doi: 10.1084/jem.180.5.1943.

DOI:10.1084/jem.180.5.1943
PMID:7964470
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2191717/
Abstract

During viral infections, CD8+,CD45RO+ T populations expand. These primed cells express abundant levels of cytoplasmic granules that contain perforin and TIA-1. Recent work has suggested that the majority of this CD8+ population downregulates Bcl-2 protein expression and is destined to undergo apoptosis. In this study we have investigated the elimination of these apoptotic CD8+ T cells by both human monocyte-derived and murine bone marrow macrophages. We have found that these phagocytes recognize and ingest both apoptotic CD8+ and CD4+ T cells using an alpha v beta 3 (vitronectin receptor)/CD36/thrombospondin recognition system, with the same receptors being used in the recognition of apoptotic neutrophils. These data provide new evidence for a mechanism that enables the clearance of greatly increased populations of CD8+ effector cells which are found during viral infections. This enables cellular homeostasis to occur in the host upon resolution of viral diseases in vivo.

摘要

在病毒感染期间，CD8 +、CD45RO + T细胞群体扩增。这些致敏细胞表达大量含有穿孔素和TIA - 1的细胞质颗粒。最近的研究表明，大多数此类CD8 +群体下调Bcl - 2蛋白表达并注定会发生凋亡。在本研究中，我们研究了人单核细胞衍生的巨噬细胞和小鼠骨髓巨噬细胞对这些凋亡CD8 + T细胞的清除作用。我们发现，这些吞噬细胞使用αvβ3（玻连蛋白受体）/CD36/血小板反应蛋白识别系统识别并吞噬凋亡的CD8 +和CD4 + T细胞，识别凋亡中性粒细胞时使用相同的受体。这些数据为一种机制提供了新证据，该机制能够清除在病毒感染期间发现的大量增加的CD8 +效应细胞群体。这使得在体内病毒疾病消退后宿主细胞能够实现稳态。