| First Author | Qiao G | Year | 2012 |
| Journal | Clin Immunol | Volume | 143 |
| Issue | 2 | Pages | 128-33 |
| PubMed ID | 22459706 | Mgi Jnum | J:183532 |
| Mgi Id | MGI:5318892 | Doi | 10.1016/j.clim.2012.02.006 |
| Citation | Qiao G, et al. (2012) Program death-1 regulates peripheral T cell tolerance via an anergy-independent mechanism. Clin Immunol 143(2):128-33 |
| abstractText | Program death-1 (PD-1) has been documented to negatively regulate immune responses. However, the cellular and molecular mechanisms for PD-1-mediated immune suppression have not been fully elucidated. In this study, we show that loss of PD-1 does not lead to defective induction of CD4(+) T cell anergy in vitro and in vivo. Rather, the absence of PD-1 inhibits the development of inducible CD4(+)Foxp3(+) regulatory T cells (iTregs) induced by TGF-beta in vitro. In support of this finding, PD-1 deficiency impairs the generation of iTregs in vivo and leads to development of severe T cell-transfer-induced colitis. Mechanistically, defective iTreg generation in the absence of PD-1 was attributed to the heightened phosphorylation of Akt. Therefore, we first demonstrate that PD-1 controls peripheral T cell tolerance via an anergy-independent but iTreg-dependent mechanism. |
