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The Journal of Immunology, 2001, 167: 6877-6883.
Copyright © 2001 by The American Association of Immunologists

A Mandatory Role for STAT4 in IL-12 Induction of Mouse T Cell CCR51

Masayuki Iwasaki, Takao Mukai, Chigusa Nakajima, Yi-Fu Yang, Ping Gao, Nobuya Yamaguchi, Michio Tomura, Hiromi Fujiwara2 and Toshiyuki Hamaoka

Department of Oncology (C6), Osaka University Graduate School of Medicine, Osaka, Japan

IL-12 was recently shown to induce CCR5 on TCR-triggered mouse T cells. Considering that STAT4 is the most critical of IL-12 signaling molecules, this study investigated the role for STAT4 in the induction of CCR5 expression. IL-12R was induced by stimulation with anti-CD3 plus anti-CD28 mAb similarly on T cells from wild-type (WT) and STAT4-deficient (STAT4-/-) mice, but the levels of IL-12R induced on IFN-{gamma}-deficient (IFN-{gamma}-/-) T cells were lower compared with WT T cells. Exposure of TCR-triggered WT T cells to IL-12 induced CCR5 expression. In contrast, TCR-triggered STAT4-/- T cells failed to express CCR5 in response to IL-12. IL-12 stimulation induced detectable albeit reduced levels of CCR5 expression on IFN-{gamma}-/- T cells. Addition of rIFN-{gamma} to cultures of IFN-{gamma}-/- T cells, particularly to cultures during TCR triggering resulted in restoration of CCR5 expression. However, CCR5 expression was not induced in STAT4-/- T cells by supplementation of rIFN-{gamma}. These results indicate that for the induction of CCR5 on T cells, 1) STAT4 plays an indispensable role; 2) such a role is not substituted by simply supplementing rIFN-{gamma}; and 3) IFN-{gamma} amplifies CCR5 induction depending on the presence of STAT4.




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