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Interleukin‐7 enhances memory CD8 + T‐cell recall responses in health but its activity is impaired in human immunodeficiency virus infection
Author(s) -
O’Connor Alison M.,
Crawley Angela M.,
Angel Jonathan B.
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2010.03325.x
Subject(s) - immune system , immunology , cytotoxic t cell , cd8 , memory t cell , biology , antigen , t cell , interleukin 7 receptor , interleukin 15 , interleukin 2 , virology , interleukin , cytokine , il 2 receptor , in vitro , biochemistry
Summary Memory CD8 + T cells regain function during a recall response, but the requirement of signals in addition to antigen during a secondary immune response is unknown. In this study, the ability of interleukin‐7 (IL‐7) to enhance memory CD8 + CD45RA − CD127 + T‐cell responses in health and in human immunodeficiency virus (HIV) infection was investigated. CD8 + T‐cell‐depleted peripheral blood mononuclear cells (PBMCs) from HIV − and untreated HIV + donors were pulsed with a cytomegalovirus/Epstein–Barr virus/influenza (CEF) peptide pool, and co‐cultured with autologous memory CD8 + T cells in the presence of IL‐7. Cell survival and the function of memory CD8 + T‐cell subsets were then evaluated. Memory CD8 + T‐cell proliferation and interferon‐γ (IFN‐γ) production was enhanced by the presence of antigen, and the addition of IL‐7 further enhanced antigen‐induced proliferation. In HIV + individuals, the presence of antigen enhanced IFN‐γ production to a small degree but did not enhance proliferation. Lastly, IL‐7 did not enhance antigen‐mediated proliferation of memory CD8 + T cells from HIV + individuals. IL‐7 therefore appears to have a role in secondary immune responses and its activity is impaired in memory CD8 + T cells from HIV + individuals. These results further our understanding of the signals involved in secondary immune responses, and provide new insight into the loss of CD8 + T‐cell function in HIV infection.