| First Author | Soper DM | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 7 | Pages | 1817-26 |
| PubMed ID | 17559173 | Mgi Jnum | J:123613 |
| Mgi Id | MGI:3718914 | Doi | 10.1002/eji.200737101 |
| Citation | Soper DM, et al. (2007) IL-2Rbeta links IL-2R signaling with Foxp3 expression. Eur J Immunol 37(7):1817-26 |
| abstractText | Immunological tolerance to self antigens is a tightly regulated process. Recent work has demonstrated that the forkhead family member Foxp3 is a critical element in the differentiation and function of mouse CD4(+)CD25(+) regulatory T cells (Treg). Recent work has suggested an important role for IL-2 in the development and maintenance of Treg. To directly assess the effect of IL-2 signaling on Treg development and function, we analyzed mice that were genetically deficient in components of the IL-2 receptor (IL-2R). Mice lacking CD25 (IL-2Ralpha) displayed a slight decrease in Treg within the thymus, while peripheral numbers are unchanged. In contrast, we found that mice deficient in CD122 (IL-2Rbeta) had a profound reduction in both thymic and peripheral Treg, coinciding with more rapid development of a fatal lymphoproliferative disease. Expression of a Foxp3 transgene restored Treg and protected against the onset of autoimmunity. Thus, a signal mediated by IL-2Rbeta is essential for the development and homeostasis of Foxp3(+) Treg in vivo. |
