Journal
GENESIS
Volume 46, Issue 12, Pages 724-731Publisher
WILEY-LISS
DOI: 10.1002/dvg.20425
Keywords
TGF beta; receptor; lymphocyte; transgenesis; mouse; Smad
Categories
Funding
- INSERM Avenir Program
- INCA
- Ligue comite du Rhone [ANR-06-JC]
- ARC [3989, 3891]
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We generated a transgenic mouse strain (LSL-T beta RI(CA)) containing a latent constitutively active TGF beta type I receptor (T beta RI/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 P-actin) promoter, is repressed by a floxed transcriptional Stop (LSL, Lox-Stop-Lox). In the presence of crerecombinase, the Stop is excised to allow T beta RI(CA) transgene expression. We showed that restricted expression of T beta RI(CA) in T lymphocytes efficiently activates TGFP signaling and rescues the T-cell autoimmune disorders of TGF beta RII conditional knockouts. Unexpectedly, our study reveals that TGFP signaling upregulation controls T-cell activation but does not impair their development or their peripheral homeostasis. In addition to the information provided on TGF beta effects on T-cell biology, LSL-T beta RI(CA) mouse constitutes an attractive tool to address the effect of TGFP signaling upregulation in any cell type expressing the cre-recombinase. genesis 46:724-731, 2008. Published 2008 Wiley-Liss, Inc.
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