Open AccessCD27 and CD57 Expression Reveals Atypical Differentiation of Human Immunodeficiency Virus Type 1-Specific Memory CD8 + T Cells
Author(s) -
Aki Hoji,
Nancy Connolly,
William Buchanan,
Charles R. Rinaldo
Publication year - 2007
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00250-06
Subject(s) - cd8 , biology , cd28 , cytotoxic t cell , flow cytometry , immunology , viremia , effector , virology , virus , immunophenotyping , immune system , in vitro , genetics
The failure of human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T cells to control chronic HIV-1 infection could be due to the progressive loss of their capacities to undergo normal memory effector differentiation. We characterized and compared the expressions of CD27, CD28, CD57, and CD62L by Epstein-Barr virus (EBV)-, cytomegalovirus (CMV)-, and HIV-1-specific CD8+ T cells by six-color, eight-parameter flow cytometry. In contrast to the maturation of EBV- and CMV-specific memory CD8+ T cells, we found that HIV-1-specific CD8+ T cells did not display coordinated down-regulation of CD27 and up-regulation of CD57 and accumulated in an atypical CD27high CD57low subset. Moreover, the accumulation of CD27high CD57low HIV-1-specific CD8+ T cells was positively correlated with HIV-1 plasma viremia. The differentiation of HIV-1-specific CD8+ T cells to an effector subset is therefore impaired during chronic HIV-1 infection. This lack of normal CD8+ T-cell differentiation could contribute to the failure of cellular immune control of HIV-1 infection.