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Journal of Experimental Medicine, Vol 180, 1943-1947, Copyright © 1994 by Rockefeller University Press
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AN Akbar, J Savill, W Gombert, M Bofill, NJ Borthwick, F Whitelaw, J Grundy, G Janossy and M Salmon
Department of Clinical Immunology, Royal Free Hospital School of Medicine, London, United Kingdom.
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.
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