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Updated: Aug 9, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
Published on: March 24, 2015
Natural human interferon-alpha augments interleukin-2 production by a direct action on the activated IL-2-producing T
1Fujisaki Cell Center, Hayashibara Biochemical Laboratories, Inc., Okayama, Japan.
The production of interleukin-2 (IL-2) by Concanavalin A (ConA)-stimulated peripheral blood leukocytes (PBL) from normal human donors was enhanced by natural human interferon-alpha (IFN-alpha). The mechanism of the action of IFN-alpha on IL-2 production was studied further using cloned human leukemic T-cell lines, which produce IL-2 spontaneously and/or after mitogen stimulation. It was found that IFN-alpha alone did not stimulate IL-2 production, but increased it in the activated cells. The ability of IFN-alpha to increase IL-2 production was abrogated by the treatment of IFN-alpha preparations with specific anti-IFN-alpha antibody, and the induced IL-2 activity was completely inhibited by monoclonal antibody against human IL-2. We suggest that the augmentation by IFN-alpha of IL-2 production in the activated T cells may be one of the mechanisms attributable to the immunotherapeutic action of IFN-alpha.
The production of interleukin-2 (IL-2) by Concanavalin A (ConA)-stimulated peripheral blood leukocytes (PBL) from normal human donors was enhanced by natural human interferon-alpha (IFN-alpha). The mechanism of the action of IFN-alpha on IL-2 production was studied further using cloned human leukemic T-cell lines, which produce IL-2 spontaneously and/or after mitogen stimulation. It was found that IFN-alpha alone did not stimulate IL-2 production, but increased it in the activated cells. The ability of IFN-alpha to increase IL-2 production was abrogated by the treatment of IFN-alpha preparations with specific anti-IFN-alpha antibody, and the induced IL-2 activity was completely inhibited by monoclonal antibody against human IL-2. We suggest that the augmentation by IFN-alpha of IL-2 production in the activated T cells may be one of the mechanisms attributable to the immunotherapeutic action of IFN-alpha.
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