Abstract：
: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.
journal_name
Immunologyjournal_title
Immunologyauthors
O'Connor AM,Crawley AM,Angel JBdoi
10.1111/j.1365-2567.2010.03325.xsubject
Has Abstractpub_date
2010-12-01 00:00:00pages
525-36issue
4eissn
0019-2805issn
1365-2567pii
IMM3325journal_volume
131pub_type
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