International Immunology, Vol 10, 1149-1157, Copyright © 1998 by Oxford University Press
AD Wilson, I Redchenko, NA Williams and AJ Morgan
Greater than 90% of the human population acquire Epstein-Barr virus (EBV)
in infancy and retain a lifelong latent infection without any clinical
consequences. Nevertheless EBV has been identified as the causal agent of
infectious mononucleosis, and is associated with several tumours including
endemic Burkitt's lymphoma and B cell lymphomas in immunosupressed
patients. B cells infected with EBV are transformed in vitro and grow
continuously as lymphoblastoid cell lines. The growth of EBV-transformed B
cells in vivo is controlled by the immune system. Studies on immunity to
EBV have mainly focused on MHC class I-restricted CD8+ cytotoxic T cells
specific for viral latent antigens. Here it is reported that in vitro
stimulation of peripheral blood lymphocytes by autologous EBV-infected B
cells, which have been induced to express lytic cycle antigens, gives rise
to a predominantly CD4+ T cell response. Furthermore, the growth of
EBV-infected B cells can also be regulated by these activated CD4+ T cells
through apoptosis mediated by CD95-CD95 ligand (CD95L). CD95-CD95L-mediated
apoptosis is an important mechanism of normal B cell growth regulation. As
EBV- transformed B cells remain susceptible to this mechanism, the control
of EBV in vivo may be not only by virus-specific CD8+ cytotoxic T cell
immunity but also by normal mechanisms of immune regulation of B cell
growth.
ARTICLES
CD4+ T cells inhibit growth of Epstein-Barr virus-transformed B cells through CD95-CD95 ligand-mediated apoptosis
Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, UK.
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