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Clonal Expansion of Double-Positive Intraepithelial Lymphocytes by MHC Class I-Related Chain A Expressed in Mouse Small Intestinal Epithelium ¹

Eun Jeong Park^*,||,#, Ichiro Takahashi^*,, Junko Ikeda, Kazuko Kawahara, Tetsuji Okamoto, Mi-Na Kweon^*,#, Satoshi Fukuyama^||,#, Veronika Groh, Thomas Spies, Yuichi Obata, Jun-Ichi Miyazaki^¶ and Hiroshi Kiyono^2,*,||,#

^* Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; Departments of Preventive Dentistry and Molecular Oral Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan; Fred Hutchinson Cancer Research Center, Clinical Research Division, Seattle, WA 98109; Department of Biological System, RIKEN BioResource Center, Tsukuba, Japan; ^¶ Division of Stem Cell Regulation Research, Osaka University Medical School, Osaka, Japan; ^|| Core Research for Engineering, Science, and Technology, Japan Science and Technology, Tokyo, Japan; and ^# Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, University of Tokyo, Tokyo, Japan

Expression of a distant homologue MHC class I molecule, MHC class I-related chain A (MICA), has been found to be stress inducible and limited to the intestinal epithelium. This nonclassical MHC molecule is associated with various carcinomas in humans. To understand the biological consequences of MICA expression in the gut, we generated transgenic (Tg) mice (T3^b-MICA Tg) under the control of the T3^b promoter. The T3^b-MICA Tg mice expressed MICA selectively in the intestine and had an increased number of TCR CD4CD8, double-positive (DP) intraepithelial lymphocytes (IELs) in the small bowel. These MICA-expanded DP IELs exhibited a bias to V8.2 and overlapped motifs of the complementarity-determining region 3 region among various Tg mice. Hence, the overexpression of MICA resulted in a clonal expansion of DP IELs. Studies in model of inflammatory bowel disease showed that transgenic MICA was able to attenuate the acute colitis induced by dextran sodium sulfate administration. Therefore, this unique in vivo model will enable investigation of possible influences of stress-inducible MICA on the gut immune surveillance.

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