Rifa'i Muhaimin, Kawamoto Yoshiyuki, Nakashima Izumi, Suzuki Haruhiko
Dept. of Immunology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
J Exp Med. 2004 Nov 1;200(9):1123-34. doi: 10.1084/jem.20040395.
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 beta 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.
免疫系统的调节对于防止免疫攻击自身成分至关重要。缺乏白细胞介素（IL）-2/IL-15受体β链（CD122）的小鼠是此类免疫攻击的模型动物，其特征是有大量异常活化的T细胞。在此，我们表明将CD8⁺CD122⁺细胞转移到缺乏CD122的新生小鼠中可完全阻止异常T细胞的发育。此外，接受野生型小鼠来源的CD8⁺CD122⁻细胞的重组激活基因-2⁻/⁻小鼠在细胞转移后10周内死亡，这表明在缺乏CD8⁺CD122⁺T细胞的情况下，正常的CD8⁺CD122⁻细胞会变成危险的活化T细胞。CD8⁺CD122⁺细胞在体内和体外均可控制活化的CD8⁺或CD4⁺T细胞。我们的结果表明，CD8⁺CD122⁺群体包括天然存在的CD8⁺调节性T细胞，可控制潜在危险的T细胞。
