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IL-4-Producing NK1.1⁺ T Cells Are Resistant to Glucocorticoid-Induced Apoptosis: Implications for the Th1/Th2 Balance¹

Koji Tamada^2,*, Mamoru Harada, Koichiro Abe^*, Tieli Li^* and Kikuo Nomoto^*

^* Department of Immunology and Department of Virology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan

To elucidate the mechanisms by which glucocorticoids promote Th2-type responses, we investigated the influence of dexamethasone (DEX) on both cytokine production and viability of NK1.1⁺ T cells. The in vivo administration of DEX enhanced the IL-4 production of spleen cells and liver mononuclear cells in wild-type mice, but not in ß₂m-deficient mice. DEX reduced the cellularity of conventional T cells, but not that of NK1.1⁺ T cells, in both spleen and liver, suggesting an increased proportion of NK1.1⁺ T cells. Moreover, the proportion of IL-4-producing NK1.1⁺ T cells increased in the DEX-injected mice. These results suggest that DEX induced IL-4 production through the preferential survival of IL-4-producing NK1.1⁺ T cells. In investigating the reason for the preferential survival of NK1.1⁺ T cells, we found that NK1.1⁺ T cells were resistant to DEX-induced apoptosis and expressed a higher level of intracellular Bcl-2 compared with conventional NK1.1^- T cells. In addition, splenic and hepatic NK1.1⁺ T cells were resistant to radiation-induced apoptosis. Collectively, our findings revealed an important role for NK1.1⁺ T cells in the regulation of Th1/Th2 balance by glucocorticoids and their possible functions under various apoptotic stimuli.

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