| First Author | King CG | Year | 2006 |
| Journal | Nat Med | Volume | 12 |
| Issue | 9 | Pages | 1088-92 |
| PubMed ID | 16921377 | Mgi Jnum | J:131909 |
| Mgi Id | MGI:3774807 | Doi | 10.1038/nm1449 |
| Citation | King CG, et al. (2006) TRAF6 is a T cell-intrinsic negative regulator required for the maintenance of immune homeostasis. Nat Med 12(9):1088-92 |
| abstractText | TRAF6 has a key role in the regulation of innate immune responses by mediating signals from both TNF receptor and interleukin-1 receptor/Toll-like receptor superfamilies. Here we show that T cell-specific deletion of TRAF6 unexpectedly results in multiorgan inflammatory disease. TRAF6-deficient T cells exhibit hyperactivation of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway compared with wild-type T cells and, as a result, become resistant to suppression by CD4+ CD25+ regulatory T cells. These data identify a previously unrecognized role for TRAF6 in the maintenance of peripheral tolerance, and suggest the presence of a T cell-intrinsic control mechanism to render responder T cells susceptible to tolerizing signals. |
