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The Journal of Immunology, 2004, 173: 6526-6531.
Copyright © 2004 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: TGF-{beta} Signaling Is Required for the In Vivo Expansion and Immunosuppressive Capacity of Regulatory CD4+CD25+ T Cells1

Samuel Huber2,*, Christoph Schramm2,3,*, Hans A. Lehr{dagger}, Amrit Mann*, Steffen Schmitt{ddagger}, Christoph Becker*, Martina Protschka*, Peter R. Galle*, Markus F. Neurath* and Manfred Blessing*,§

* I. Medizinische Klinik, {dagger} Institut für Pathologie, {ddagger} Naturwissenschaftlich-Medizinisches Forschungszentrum, Johannes Gutenberg-Universität, Mainz, Germany; and § Biotechnologisch Biomedizinisches Zentrum, Universität Leipzig, Leipzig, Germany

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.




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