| Literature DB >> 15331707 |
Marcin Moniuszko1, Terry Fry, Wen-Po Tsai, Michel Morre, Brigitte Assouline, Pierre Cortez, Mark G Lewis, Scott Cairns, Crystal Mackall, Genoveffa Franchini.
Abstract
Interleukin-7 (IL-7) regulates T-cell homeostasis, and its availability is augmented in lymphopenic hosts. Naive CD8+ T cells transferred to lymphopenic mice acquire a memory-like phenotype, raising the possibility that IL-7 is the biological mediator of this effect. Here, we provide direct evidence that IL-7 induces the acquisition of memory-cell markers not only in CD8+ T cells but also in CD4+ T-cell subsets in immune-competent Indian rhesus macaques. The increase of these memory-like populations was dependent on the dose of the cytokine, and these cells were found in the blood as well as secondary lymphoid organs. Memory-like CD4+ and CD8+ T cells acquired the ability to secrete tumor necrosis factor alpha and, to a lesser extent, gamma interferon following stimulation with a cognate antigen. The phenotypic change observed in naive T cells was promptly reversed after discontinuation of IL-7. Importantly, IL-7 induced cycling of both CD4+ and CD8+ central memory and effector memory T cells, demonstrating its contribution to the maintenance of the entire T-cell pool. Thus, IL-7 may be of benefit in the treatment of iatrogenic or virus-induced T-cell depletion. Copyright 2004 American Society for MicrobiologyEntities:
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Year: 2004 PMID: 15331707 PMCID: PMC515001 DOI: 10.1128/JVI.78.18.9740-9749.2004
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103