Inhaltszusammenfassung

Data regarding the role of TGF-beta for the in vivo function of regulatory CD4( )CD25( ) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta 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 transferrin...Data regarding the role of TGF-beta for the in vivo function of regulatory CD4( )CD25( ) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta 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-beta 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-beta signaling in CD4( )CD25( ) Treg is required for their in vivo expansion and suppressive capacity.» weiterlesen» einklappen

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DDC Sachgruppe:
Medizin