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International Immunology, Vol. 15, No. 6, pp. 741-749, June 2003
© 2003 Japanese Society for Immunology

Critical function of T cell death-associated gene 8 in glucocorticoid-induced thymocyte apoptosis

Noriko Tosa1,3, Masaaki Murakami1, Wen Yi Jia1, Minesuke Yokoyama4, Taro Masunaga1, Chikako Iwabuchi2, Manabu Inobe1, Kazuya Iwabuchi2, Tadaaki Miyazaki1, Kazunori Onoe2, Makoto Iwata4 and Toshimitsu Uede1

Divisions of 1 Molecular Immunology and 2 Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo, Hokkaido 060-8638, Japan 3 Immuno-Biological Laboratories Co., Ltd, Fujioka, Gunma 375-0005, Japan 4 Mitsubishi Kagaku Institute of Life Sciences, Machida, Tokyo 194-8511, Japan

Correspondence to: N. Tosa; E-mail: tosa{at}imm.hokudai.ac.jp
Transmitting editor: T. Hamaoka

Transcriptional expression of a gene or genes is absolutely required for induction of glucocorticoid-induced thymocyte apoptosis. We have previously shown that expression of T cell death-associated gene 8 (TDAG8) is quickly induced exclusively in the thymus after dexamethasone (DEX) treatment. Here, we present data that TDAG8 expression is induced prior to induction of DEX-mediated apoptosis. In contrast, TDAG8 expression in thymocytes was not induced in the process of {gamma}-irradiation-mediated apoptosis. TDAG8 expression accelerated only DEX-induced, but not TCR-mediated or {gamma}-irradiation-induced, thymocyte apoptosis in transgenic mice overexpressing TDAG8. Interestingly, these effects were specifically detected in CD4+CD8+ double-positive thymocytes. Moreover, activation of caspase-3, -8 and -9 was enhanced in thymocytes of TDAG8 transgenic mice after DEX stimulation. In conclusion, TDAG8 expression is involved in glucocorticoid-induced signals to activate caspase-9, -8 and -3 for subsequent apoptosis induction in CD4+CD8+ double-positive thymocytes.

Keywords: apoptosis, dexamethasone, development, T lymphocyte, thymus


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