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Failing immune control as a result of impaired CD8+ T-cell maturation: CD27 might provide a clue
Debbie van Baarle1, Stefan Kostense, Marinus H J van Oers
1Dept of Clinical Viro-Immunology, Sanquin Research at CLB & Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, The Netherlands. d_van_baarle@clb.nl
Despite readily detectable virus-specific CD8(+) T cells in most HIV-infected patients, immune surveillance is eventually lost, leading to progression to AIDS. Recently developed insights into human T-cell differentiation have been used to study the phenotype of virus-specific T cells in HIV-infected individuals. Based on these results, we propose that failing immune control in human viral infection could be a result of impaired cytotoxic T-lymphocyte (CTL) maturation into fully differentiated effector T cells. Impaired maturation is not confined to HIV-specific CD8(+) T cells but could also be involved in failing immunity to Epstein-Barr virus and other viral infections. We postulate that CD27(-) effector CD8(+) T cells might be required for adequate control of chronic viral infection and prevention of disease development.
Despite readily detectable virus-specific CD8(+) T cells in most HIV-infected patients, immune surveillance is eventually lost, leading to progression to AIDS. Recently developed insights into human T-cell differentiation have been used to study the phenotype of virus-specific T cells in HIV-infected individuals. Based on these results, we propose that failing immune control in human viral infection could be a result of impaired cytotoxic T-lymphocyte (CTL) maturation into fully differentiated effector T cells. Impaired maturation is not confined to HIV-specific CD8(+) T cells but could also be involved in failing immunity to Epstein-Barr virus and other viral infections. We postulate that CD27(-) effector CD8(+) T cells might be required for adequate control of chronic viral infection and prevention of disease development.
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