Akbar A N, Savill J, Gombert W, Bofill M, Borthwick N J, Whitelaw F, Grundy J, Janossy G, Salmon M
Department of Clinical Immunology, Royal Free Hospital School of Medicine, London, United Kingdom.
J Exp Med. 1994 Nov 1;180(5):1943-7. doi: 10.1084/jem.180.5.1943.
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.
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。