Cutting edge: TGF-β signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+ CD25+ T cells

S Huber, C Schramm, HA Lehr, A Mann… - The Journal of …, 2004 - journals.aai.org
S Huber, C Schramm, HA Lehr, A Mann, S Schmitt, C Becker, M Protschka, PR Galle
The Journal of Immunology, 2004journals.aai.org
Data regarding the role of TGF-β for the in vivo function of regulatory CD4+ CD25+ T cells
(Treg) are controversial. A transgenic mouse model with impaired TGF-β signaling
specifically in T cells was used to assess the role of endogenous TGF-β for the in vivo
function of CD4+ CD25+ Treg in a murine model of colitis induced by dextran sulfate.
Transfer of wild-type, but not transgenic CD4+ CD25+ Treg was found to suppress colitis in
wild-type mice. In addition, by transferring CFSE-labeled CD4+ CD25+ Treg we could …
Abstract
Data regarding the role of TGF-β for the in vivo function of regulatory CD4+ CD25+ T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-β signaling specifically in T cells was used to assess the role of endogenous TGF-β for the in vivo function of CD4+ CD25+ Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4+ CD25+ Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4+ CD25+ Treg we could demonstrate that endogenous TGF-β promotes the expansion of CD4+ CD25+ Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4+ CD25+ Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-β signaling in CD4+ CD25+ Treg is required for their in vivo expansion and suppressive capacity.
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