| First Author | Sugai M | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 11 | Pages | 6515-20 |
| PubMed ID | 21515792 | Mgi Jnum | J:173202 |
| Mgi Id | MGI:5013534 | Doi | 10.4049/jimmunol.1001671 |
| Citation | Sugai M, et al. (2011) Runx3 is required for full activation of regulatory T cells to prevent colitis-associated tumor formation. J Immunol 186(11):6515-20 |
| abstractText | Inflammation is increasingly recognized as an essential component of tumorigenesis, which is promoted and suppressed by various T cell subsets acting in different ways. It was shown previously in Runx3-deficient mice that differentiation of CD8 T and NK cells is perturbed. In this study, we show that Runx3 is also required for proper differentiation and function of regulatory T cells. In Runx3-deficient mice, T cells were unable to inhibit inflammation and to suppress tumor development. As expected, recombination activating gene 2-deficient mice bearing Runx3-deficient lymphocytes spontaneously developed colon tumors. However, tumor formation was completely blocked by transfer of either regulatory T cells or CD8 T cells derived from wild-type mice to mutant mice or by housing mutant mice in a specific pathogen-free condition. These results indicate that Runx3-deficient lymphocytes and microorganisms act together to induce inflammation and consequently induce the development of colon tumors. |
