| First Author | Donkor MK | Year | 2011 |
| Journal | Immunity | Volume | 35 |
| Issue | 1 | Pages | 123-34 |
| PubMed ID | 21757379 | Mgi Jnum | J:174515 |
| Mgi Id | MGI:5139923 | Doi | 10.1016/j.immuni.2011.04.019 |
| Citation | Donkor MK, et al. (2011) T Cell Surveillance of Oncogene-Induced Prostate Cancer Is Impeded by T Cell-Derived TGF-beta1 Cytokine. Immunity 35(1):123-34 |
| abstractText | Tolerance induction in T cells takes place in most tumors and is thought to account for tumor evasion from immune eradication. Production of the cytokine TGF-beta is implicated in immunosuppression, but the cellular mechanism by which TGF-beta induces T cell dysfunction remains unclear. With a transgenic model of prostate cancer, we showed that tumor development was not suppressed by the adaptive immune system, which was associated with heightened TGF-beta signaling in T cells from the tumor-draining lymph nodes. Blockade of TGF-beta signaling in T cells enhanced tumor antigen-specific T cell responses and inhibited tumor development. Surprisingly, T cell- but not Treg cell-specific ablation of TGF-beta1 was sufficient to augment T cell cytotoxic activity and blocked tumor growth and metastases. These findings reveal that T cell production of TGF-beta1 is an essential requirement for tumors to evade immunosurveillance independent of TGF-beta produced by tumors. |
