William Moss

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Recombinant interleukin-7 induces proliferation of naive macaque CD4+ and CD8+ T cells in vivo.

Marcin Moniuszko; Terry Fry; Wen-Po Tsai; Michel Morre; Brigitte Assouline; Pierre Cortez; Mark G Lewis; Scott Cairns; Crystal Mackall; Genoveffa Franchini (Profiled Author: Crystal Mackall)

Animal Models and Retroviral Vaccines Section, National Cancer Institute, Bldg. 41, Rm. D804, Bethesda, MD 20892-5065, USA.
Journal of virology 2004;78(18):9740-9.

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.

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