Failing immune control as a result of impaired CD8+ T-cell maturation: CD27 might provide a clue.
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.
van Baarle
Debbie
D
Dept 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
Kostense
Stefan
S
van Oers
Marinus H J
MH
Hamann
Dorte
D
Miedema
Frank
F
D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D002454:Cell Differentiation; D020031:Epstein-Barr Virus Infections / Q000276:immunology / Q000473:pathology; D015658:HIV Infections / Q000276:immunology / Q000473:pathology; D006801:Humans; D018448:Models, Immunological; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000473:pathology; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000378:metabolism*; D014777:Virus Diseases / Q000276:immunology* / Q000473:pathology
D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7