Tryptophan catabolism is a tolerogenic effector system in regulatory T cell function, yet the general mechanisms whereby tryptophan catabolism affects T cell responses remain unclear. We provide evidence that its effects include the emergence of a regulatory phenotype in naive CD4(+)CD25(-) cells via the general control non-depressing 2 (GCN2) protein kinase mediated induction of the forkhead transcription factor Foxp3. These cells are capable of effective control of diabetogenic T cells in vivo.

Tryptophan catabolism generates autoimmune-preventive regulatory T cells

FALLARINO, Francesca
;
GROHMANN, Ursula;VACCA, Carmine;ORABONA, Ciriana;BIANCHI, Roberta;BELLADONNA, Maria Laura;VOLPI, CLAUDIA;FIORETTI, Maria Cristina;PUCCETTI, Paolo
2006

Abstract

Tryptophan catabolism is a tolerogenic effector system in regulatory T cell function, yet the general mechanisms whereby tryptophan catabolism affects T cell responses remain unclear. We provide evidence that its effects include the emergence of a regulatory phenotype in naive CD4(+)CD25(-) cells via the general control non-depressing 2 (GCN2) protein kinase mediated induction of the forkhead transcription factor Foxp3. These cells are capable of effective control of diabetogenic T cells in vivo.
2006
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/152771
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