| First Author | King CG | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 1 | Pages | 34-8 |
| PubMed ID | 18097000 | Mgi Jnum | J:130882 |
| Mgi Id | MGI:3772503 | Doi | 10.4049/jimmunol.180.1.34 |
| Citation | King CG, et al. (2008) Cutting edge: requirement for TRAF6 in the induction of T cell anergy. J Immunol 180(1):34-8 |
| abstractText | TRAF6, TNFR-associated factor 6, is a key adaptor downstream from the TNF receptor and TLR superfamily members. T cell-specific deletion of TRAF6 (TRAF6-DeltaT) was recently shown to result in the development of multiorgan inflammatory disease and the resistance of responder T cells to suppression by CD4+CD25+ regulatory T cells. In this study we examined the role of TRAF6 in an additional mechanism of peripheral tolerance, anergy. We have determined that the loss of TRAF6 restores the ability of CD28-/- T cells to proliferate and produce IL-2. Consistent with this, TRAF6-DeltaT T cells were resistant to anergizing signals both in vitro and in vivo. Resistance to anergy was correlated with decreased expression of Cbl-b. These findings reveal that in addition to its role in rendering T cells susceptible to control by CD4+CD25+ regulatory T cells, TRAF6 is essential for the induction of T cell anergy, implicating TRAF6 as a critical mediator of peripheral tolerance. |
