| First Author | Guo L | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 1 | Pages | 71-80 |
| PubMed ID | 19877010 | Mgi Jnum | J:155697 |
| Mgi Id | MGI:4415107 | Doi | 10.1002/eji.200939404 |
| Citation | Guo L, et al. (2010) Inhibition of clonal expansion by Foxp3 expression as a mechanism of controlled T-cell responses and autoimmune disease. Eur J Immunol 40(1):71-80 |
| abstractText | The essential role of the transcription factor Foxp3 in the development and function of Treg has been well documented. The role of Foxp3 in non-Treg, however, is not fully understood. Emerging evidence indicates that Foxp3 expression is not confined to CD4+CD25+ Treg. The present study shows that in Foxp3 transgenic (Foxp3-Tg) mice, in which the transgene is driven by the lck distal promoter, CD4+CD25- T cells that express the Foxp3 transgene do not upregulate the expression of CD25-, GITR, or CTLA-4, and do not have suppressive function; however, the Foxp3-Tg+CD4+CD25- T cells exhibit significantly reduced proliferative response to TCR engagement. Foxp3-Tg mice are resistant to collagen-induced arthritis via reduced cellular proliferation of activated T cells. These findings indicate that Foxp3 upregulation in activated non-Treg may be a mechanism to suppress immune responses by reduced clonal expansion of activated T cells. |
