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¹ Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
² Brawijaya University, Malang 65145, East Java, Indonesia

Address correspondence to Haruhiko Suzuki, Dept. of Immunology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Phone: 81-52-744-2135; Fax: 81-52-744-2972; email: k46200a{at}nucc.cc.nagoya-u.ac.jp

Regulation of immune system is of paramount importance to prevent immune attacks against self-components. Mice deficient in the interleukin (IL)-2/IL-15 receptor ß chain, CD122, are model animals of such immune attacks and characteristically have a high number of abnormally activated T cells. Here, we show that the transfer of CD8⁺CD122⁺ cells into CD122-deficient neonates totally prevented the development of abnormal T cells. Furthermore, recombination activating gene–2^–/– mice that received wild-type mice–derived CD8⁺CD122^– cells died within 10 wk after cell transfer, indicating that normal CD8⁺CD122^– cells become dangerously activated T cells in the absence of CD8⁺CD122⁺ T cells. CD8⁺CD122⁺ cells could control activated CD8⁺ or CD4⁺ T cells both in vivo and in vitro. Our results indicate that the CD8⁺CD122⁺ population includes naturally occurring CD8⁺ regulatory T cells that control potentially dangerous T cells.

Key Words: immune regulation • CD8⁺ T cells • CD122 • T cell control • activated T cells

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