We generated a transgenic mouse strain (LSL‐TβRI^CA) containing a latent constitutively active TGFβ type I receptor (TβRI/ALK5) by using a knock‐in strategy into the X chromosome‐linked hypoxanthine phosphoribosyl‐transferase (Hprt) locus. Transgene expression, under the control of the ubiquitous CAG (human cytomegalovirus enhancer and chicken β‐actin) promoter, is repressed by a floxed transcriptional “Stop” (LSL, Lox‐Stop‐Lox). In the presence of cre‐recombinase, the “Stop” is excised to allow TβRI^CA transgene expression. We showed that restricted expression of TβRI^CA in T lymphocytes efficiently activates TGFβ signaling and rescues the T‐cell autoimmune disorders of TGFβRII conditional knockouts. Unexpectedly, our study reveals that TGFβ signaling upregulation controls T‐cell activation but does not impair their development or their peripheral homeostasis. In addition to the information provided on TGFβ effects on T‐cell biology, LSL‐TβRI^CA mouse constitutes an attractive tool to address the effect of TGFβ signaling upregulation in any cell type expressing the cre‐recombinase. genesis 46:724–731, 2008. Published 2008 Wiley‐Liss, Inc.