| First Author | Barron L | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 5 | Pages | 2762-6 |
| PubMed ID | 18292495 | Mgi Jnum | J:131729 |
| Mgi Id | MGI:3774251 | Doi | 10.4049/jimmunol.180.5.2762 |
| Citation | Barron L, et al. (2008) Cutting edge: contributions of apoptosis and anergy to systemic T cell tolerance. J Immunol 180(5):2762-6 |
| abstractText | Multiple pathways can induce and maintain peripheral T cell tolerance. The goal of this study was to define the contributions of apoptosis and anergy to the maintenance of self-tolerance to a systemic Ag. Upon transfer into mice expressing OVA systemically, OVA-specific DO11 CD4(+) T cells are activated transiently, cease responding, and die. Bim is the essential apoptosis-inducing trigger and apoptosis proceeds despite increased expression of Bcl-2 and Bcl-x. However, preventing apoptosis by eliminating Bim does not restore proliferation or cytokine production by DO11 cells. While Foxp3 is transiently induced, anergy is not associated with the stable development of regulatory T cells. Thus, apoptosis is dispensable for tolerance to a systemic self-Ag and cell-intrinsic anergy is sufficient to tolerize T cells. |
