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RESEARCH PRODUCT
Cutting Edge: TGF-β Signaling Is Required for the In Vivo Expansion and Immunosuppressive Capacity of Regulatory CD4+CD25+ T Cells
Steffen SchmittManfred BlessingChristoph SchrammPeter R. GalleChristoph BeckerMarkus F. NeurathMartina ProtschkaHans A. LehrSamuel HuberAmrit Mannsubject
Genetically modified mouseAdoptive cell transferTransgeneImmunologychemical and pharmacologic phenomenaEndogenyBiologyT-Lymphocytes RegulatoryMiceTransforming Growth Factor betaIn vivomedicineAnimalsHumansImmunology and AllergyGenetic Predisposition to DiseaseLymphocyte CountIL-2 receptorColitisReceptorCell DifferentiationReceptors Interleukin-2hemic and immune systemsColitismedicine.diseaseAdoptive TransferCell biologyImmunologySignal Transductiondescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2004-11-24 | The Journal of Immunology |