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Intestinal Intraepithelial T Lymphocytes in IL-15-Deficient Mice1
* Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; and
First Department of Surgery, Gunma University School of Medicine, Maebashi, Japan
IL-15 knockout (KO) mice have severely reduced numbers of TCR
intestinal intraepithelial T lymphocytes (i-IEL), suggesting requirements of IL-15 signaling in the development or maintenance of i-IEL. To determine an involvement of survival signals via Bcl-2 in IL-15-mediated homeostasis of TCR i-IEL, we introduced a bcl-2 transgene into IL-15 KO mice. In situ apoptosis of TCR i-IEL was decreased in Bcl-2 transgenic (Tg) x IL-15 KO mice compared with IL-15 KO mice. The enforced expression of Bcl-2 partially restored the numbers of TCR i-IEL in IL-15 KO mice. However, effector functions of TCR i-IEL, including cytokine production and cytotoxic activity, were not recovered in Bcl-2 Tg x IL-15 KO mice. Importantly, TCR i-IEL in Bcl-2 Tg x IL-15 KO mice expressed a reduced level of eomesodermin, a transcription factor critical for effector functions of NK cells and CD8+ T cells. Similar to the case of TCR i-IEL, enforced expression of Bcl-2 restored the numbers but not the functions of NK cells in IL-15 KO mice. These results suggest that Bcl-2-mediated survival signal is involved in the IL-15-mediated homeostasis of TCR i-IEL and NK cells, but other signals from IL-15 are critical for inducing transcription factors, such as eomesodermin for their effector functions.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Funds for Japan Science and Technology, Grant-in-Aid for Scientific Research on Priority Areas and Young Scientists (B), Japan Society for Promotion of Science, and grants from the Japanese Ministry of Education, Science, and Culture (to Y.Y.), Yakult Bioscience Foundation (to Y.Y.), and Uehara Memorial Foundation (to Y.Y.).
2 Address correspondence and reprint requests to Dr. Yasunobu Yoshikai, Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. E-mail address: yoshikai{at}bioreg.kyushu-u.ac.jp
3 Abbreviations used in this paper: c, common chain; i-IEL, intestinal intraepithelial T lymphocyte; s-IEL, skin intraepithelial T lymphocyte; KO, knockout; Tg, transgenic.
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