Requirement for IRF-1 in the microenvironment supporting development of natural killer cells

Kouetsu Ogasawara, Shigeaki Hida, Nazli Azimi, Yutaka Tagaya, Takeo Sato, Taeko Yokochi-Fukuda, Thomas A. Waldmann, Tadatsugu Taniguchi and Shinsuke Taki ()
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Kouetsu Ogasawara: Graduate School of Medicine and Faculty of Medicine, University of Tokyo
Shigeaki Hida: Graduate School of Medicine and Faculty of Medicine, University of Tokyo
Nazli Azimi: Metabolism Branch, National Cancer Institute, National Institutes of Health
Yutaka Tagaya: Metabolism Branch, National Cancer Institute, National Institutes of Health
Takeo Sato: Graduate School of Medicine and Faculty of Medicine, University of Tokyo
Taeko Yokochi-Fukuda: Graduate School of Medicine and Faculty of Medicine, University of Tokyo
Thomas A. Waldmann: Metabolism Branch, National Cancer Institute, National Institutes of Health
Tadatsugu Taniguchi: Graduate School of Medicine and Faculty of Medicine, University of Tokyo
Shinsuke Taki: Graduate School of Medicine and Faculty of Medicine, University of Tokyo

Nature, 1998, vol. 391, issue 6668, 700-703

Abstract: Abstract Natural killer (NK) cells are critical for both innate and adaptive immunity1,2. The development of NK cells requires interactions between their progenitors and the bone-marrow microenvironment3,4,5,6; however, little is known about the molecular nature of such interactions. Mice that do not express the transcription factor interferon-regulatory factor-1 (IRF-1; such mice are IRF-1−/− mice) have been shown to exhibit a severe NK-cell deficiency7,8. Here we demonstrate that the lack of IRF-1 affects the radiation-resistant cells that constitute the microenvironment required for NK-cell development, but not the NK-cell progenitors themselves. We also show that IRF-1−/− bone-marrow cells can generate functional NK cells whencultured with the cytokine interleukin-15 (9-12) and that the interleukin-15 gene is transcriptionally regulated by IRF-1. These results reveal, for the first time, a molecular mechanism by which the bone-marrow microenvironment supports NK-cell development.

Date: 1998
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DOI: 10.1038/35636

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