| First Author | Zhang N | Year | 2012 |
| Journal | Nat Immunol | Volume | 13 |
| Issue | 7 | Pages | 667-73 |
| PubMed ID | 22634866 | Mgi Jnum | J:187653 |
| Mgi Id | MGI:5437591 | Doi | 10.1038/ni.2319 |
| Citation | Zhang N, et al. (2012) TGF-beta signaling to T cells inhibits autoimmunity during lymphopenia-driven proliferation. Nat Immunol 13(7):667-73 |
| abstractText | T cell-specific deletion of the receptor for transforming growth factor-beta (TGF-beta) mediated by Cre recombinase expressed early in T cell development leads to early-onset lethal autoimmune disease that cannot be controlled by regulatory T cells. However, when we deleted that receptor through the use of Cre driven by a promoter that is active much later in T cell development, adult mice in which most peripheral CD4(+) or CD8(+) T cells lacked the receptor for TGF-beta showed no signs of autoimmunity. Because of their enhanced responses to weak stimulation of the T cell antigen receptor, when transferred into lymphopenic recipients, naive TGF-beta-unresponsive T cells underwent much more proliferation and differentiation into effector cells and induced lymphoproliferative disease. We propose that TGF-beta signaling controls the self-reactivity of peripheral T cells but that in the absence of TGF-beta signals, an added trigger such as lymphopenia is needed to drive overt autoimmune disease. |
