Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. (Articolo in rivista) (literal)

Anno

• 2006-01-01T00:00:00+01:00 (literal)

Alternative label

• Romani L., Bistoni F.a, Perruccio K., Montagnoli C., Gaziano R., Bozza S., Bonifazi P., Bistoni G., Rasi G.b, Velardi A., Fallarino F., Garaci E c., Puccetti P. (2006)
  Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance.
  in Blood
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Romani L., Bistoni F.a, Perruccio K., Montagnoli C., Gaziano R., Bozza S., Bonifazi P., Bistoni G., Rasi G.b, Velardi A., Fallarino F., Garaci E c., Puccetti P. (literal)

Pagina inizio

• 2265 (literal)

Pagina fine

• 2274 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni

• Impact Factor = 10.37 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 108/7 (literal)

Rivista

• Blood (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• a = Dept. of Experimental Medicine, Section of Microbiology, University of Perugia, Via del Giochetto, Perugia 06126, Italy; b = Institute of Neurobiology and Molecular Medicine, CNR, Research Area of Tor Vergata, Rome, Italy; c = Faculty of Medicine and Surgery, Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Rome, Italy (literal)

Titolo

• Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. (literal)

Abstract

• Thymosin alpha1 (Talpha1), a naturally occurring thymic peptide, primes dendritic cells (DCs) for antifungal T-helper type 1 resistance through Toll-like receptor 9 (TLR9) signaling. As TLR9 signaling also activates the immuno-suppressive pathway of tryptophan catabolism via indoleamine 2,3-dioxygenase (IDO), we examined Talpha1 for possible induction of DC-dependent regulatory effects. Talpha1 affected T-helper cell priming and tolerance induction by human and murine DCs and induced IDO expression and function in the latter cells. IDO activation by Talpha1 required TLR9 and type I interferon receptor signaling and resulted in interleukin-10 production and generation of regulatory T cells. In transfer experiments, functionally distinct subsets of differentiated DCs were required for priming and tolerance to a fungal pathogen or alloantigens. In contrast, Talpha1-primed DCs fulfilled multiple requirements, including the induction of T-helper type 1 immunity within a regulatory environment. Thus, instructive immunotherapy with Talpha1 targeting IDO-competent DCs could allow for a balanced control of inflammation and tolerance. (literal)

Prodotto di

• Patologie infettive, infiammatorie e degenerative (ME.P04.005.001) (Modulo)
• Istituto di neurobiologia e medicina molecolare (INMM) (Istituto)

Autore CNR

• GUIDO RASI (Persona)

Incoming links:

Autore CNR di

• GUIDO RASI (Persona)

Prodotto

• Istituto di neurobiologia e medicina molecolare (INMM) (Istituto)
• Patologie infettive, infiammatorie e degenerative (ME.P04.005.001) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Blood (Rivista)