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Mucosal T Cells Bearing TCR Play a Protective Role in Intestinal Inflammation¹

Kyoko Inagaki-Ohara^2,*,, Takatoshi Chinen, Goro Matsuzaki, Atsuo Sasaki, Yukiko Sakamoto^*, Kenji Hiromatsu^*, Fukumi Nakamura-Uchiyama^*, Yukifumi Nawa^* and Akihiko Yoshimura^2,

^* Department of Infectious Diseases, Division of Parasitic Disease, University of Miyazaki, Miyazaki Medical College, Kiyotake, Miyazaki, Japan; Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Maidashi, Fukuoka, Japan; and Division of Molecular Microbiology, Center of Molecular Biosciences, University of the Ryukyus, Senbaru, Nishihara, Okinawa, Japan

Intestinal intraepithelial lymphocytes (IEL) bearing TCR represent a major T cell population in the murine intestine. However, the role of IEL in inflammatory bowel diseases (IBD) remains controversial. In this study, we show that IEL is an important protective T cell population against IBD. T cell-deficient (C^–/–) mice developed spontaneous colitis with age and showed high susceptibility to Th1-type 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis at a young age. Transfer of IEL to C^–/– mice ameliorated TNBS-induced colitis, which correlated with decrease of IFN- and TNF- production and an increase of TGF- production by IEL. Furthermore, a high level of IL-15, which inhibits activation-induced cell death to terminate inflammation, was expressed more in intestinal epithelial cells (EC) from TNBS-treated C^–/– mice than in those from wild-type mice. EC from wild-type mice significantly suppressed the IFN- production of IEL from TNBS-treated C^–/– mice, whereas EC from TNBS-treated C^–/– mice did not. These data indicate that IEL play important roles in controlling IBD by regulating mucosal T cell activation cooperated with EC function. Our study suggests that enhancement of regulatory T cell activity is a possible new cell therapy for colitis.

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