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IWASAKI Masayuki
Department Research Institutes and Facilities, Research Institutes and Facilities Position Assistant Professor |
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| Article types | Original article |
| Language | English |
| Peer review | Peer reviewed |
| Title | A mandatory role for STAT4 in IL-12 induction of mouse T cell CCR5. |
| Journal | Formal name：Journal of immunology (Baltimore, Md. : 1950) Abbreviation：J Immunol ISSN code：00221767/00221767 |
| Domestic / Foregin | Foregin |
| Volume, Issue, Page | 167(12),pp.6877-83 |
| Author and coauthor | Iwasaki M, Mukai T, Nakajima C, Yang Y F, Gao P, Yamaguchi N, Tomura M, Fujiwara H, Hamaoka T |
| Authorship | Lead author |
| Publication date | 2001/12 |
| Summary | 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. |
| DOI | 10.4049/jimmunol.167.12.6877 |
| PMID | 11739505 |