| First Author | Fahlén L | Year | 2005 |
| Journal | J Exp Med | Volume | 201 |
| Issue | 5 | Pages | 737-46 |
| PubMed ID | 15753207 | Mgi Jnum | J:96624 |
| Mgi Id | MGI:3531052 | Doi | 10.1084/jem.20040685 |
| Citation | Fahlen L, et al. (2005) T cells that cannot respond to TGF-{beta} escape control by CD4+CD25+ regulatory T cells. J Exp Med 201(5):737-46 |
| abstractText | CD4(+)CD25(+) regulatory T (T reg) cells play a pivotal role in control of the immune response. Transforming growth factor-beta (TGF-beta) has been shown to be required for T reg cell activity; however, precisely how it is involved in the mechanism of suppression is poorly understood. Using the T cell transfer model of colitis, we show here that CD4(+)CD45RB(high) T cells that express a dominant negative TGF-beta receptor type II (dnTbetaRII) and therefore cannot respond to TGF-beta, escape control by T reg cells in vivo. CD4(+)CD25(+) T reg cells from the thymus of dnTbetaRII mice retain the ability to inhibit colitis, suggesting that T cell responsiveness to TGF-beta is not required for the development or peripheral function of thymic-derived T reg cells. In contrast, T reg cell activity among the peripheral dnTbetaRII CD4(+)CD25(+) population is masked by the presence of colitogenic effector cells that cannot be suppressed. Finally, we show that CD4(+)CD25(+) T reg cells develop normally in the absence of TGF-beta1 and retain the ability to suppress colitis in vivo. Importantly, the function of TGF-beta1(-/-) T reg cells was abrogated by anti-TGF-beta monoclonal antibody, indicating that functional TGF-beta can be provided by a non-T reg cell source. |
