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The Journal of Immunology, 2002, 169: 6187-6192.
Copyright © 2002 by The American Association of Immunologists

Autocrine IL-15 Mediates Intestinal Epithelial Cell Death Via the Activation of Neighboring Intraepithelial NK Cells1

Naotoshi Kinoshita*, Takachika Hiroi*, Noriyuki Ohta*, Satoshi Fukuyama*, Eun Jeong Park* and Hiroshi Kiyono*

* This work was supported by grants from the Ministry of Education, Science, Sports, and Culture, the Ministry of Health and Welfare, and the Health Science Foundation, Japan. 2 Address correspondence and reprint requests to Dr. Hiroshi Kiyono, Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan. E-mail address: kiyono@biken.osaka-u.ac.jp

Intestinal intraepithelial lymphocytes (IELs), which reside between the basolateral faces of intestinal epithelial cells (IECs), provide a first-line defense against pathogens via their cytotoxic activity. Although IEC-derived IL-7 and IL-15 are key regulatory cytokines for the development and activation of IELs, we report here that IL-15 but not IL-7 mediates the reciprocal interaction between IELs and IECs, an important interaction for the regulation of appropriate mucosal immunohomeostasis. IL-15-treated IELs induced cell death in IECs via the cytotoxic activity in vitro. Among the different subsets of IL-15-treated IELs, CD4-CD8-TCR- IELs, which express NK marker (DX5 or NK1.1), showed the most potent syngenic IEC killing activity. These intraepithelial NK cells expressed Ly-49 molecules, NKG2 receptors, and perforin. These results suggest the possibility that the cell death program of IECs could be regulated by self-produced IL-15 through the activation of intraepithelial NK cells.




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