By restraining T-cell activation and promoting Treg-cell expansion, myeloid-derived suppressor cells (MDSCs) and tolerogenic DCs can control self-reactive and antigraft effector T cells in autoimmunity and transplantation. Their therapeutic use and characterization, however, is limited by their scarce availability in the peripheral blood of tumor-free donors. In the present study, we describe and characterize a novel population of human myeloid suppressor cells, named fibrocytic MDSC, which are differentiated from umbilical cord blood precursors by 4-day culture with FDA-approved cytokines (recombinant human-GM-CSF and recombinant human-G-CSF). This MDSC subset, characterized by the expression of MDSC-, DC-, and fibrocyte-associated markers, promotes Treg-cell expansion and induces normoglycemia in a xenogeneic mouse model of Type 1 diabetes. In order to exert their protolerogenic function, fibrocytic MDSCs require direct contact with activated T cells, which leads to the production and secretion of IDO. This new myeloid subset may have an important role in the in vitro and in vivo production of Treg cells for the treatment of autoimmune diseases, and in either the prevention or control of allograft rejection.

Human fibrocytic myeloid-derived suppressor cells express IDO and promote tolerance via Treg-cell expansion / Zoso, Alessia; Mazza, Emilia Maria Cristina; Bicciato, Silvio; Mandruzzato, Susanna; Bronte, Vincenzo; Serafini, Paolo; Inverardi, Luca. - In: EUROPEAN JOURNAL OF IMMUNOLOGY. - ISSN 0014-2980. - ELETTRONICO. - 44:(2014), pp. 3307-19-3319. [10.1002/eji.201444522]

Human fibrocytic myeloid-derived suppressor cells express IDO and promote tolerance via Treg-cell expansion

MAZZA, Emilia Maria Cristina;BICCIATO, Silvio;
2014

Abstract

By restraining T-cell activation and promoting Treg-cell expansion, myeloid-derived suppressor cells (MDSCs) and tolerogenic DCs can control self-reactive and antigraft effector T cells in autoimmunity and transplantation. Their therapeutic use and characterization, however, is limited by their scarce availability in the peripheral blood of tumor-free donors. In the present study, we describe and characterize a novel population of human myeloid suppressor cells, named fibrocytic MDSC, which are differentiated from umbilical cord blood precursors by 4-day culture with FDA-approved cytokines (recombinant human-GM-CSF and recombinant human-G-CSF). This MDSC subset, characterized by the expression of MDSC-, DC-, and fibrocyte-associated markers, promotes Treg-cell expansion and induces normoglycemia in a xenogeneic mouse model of Type 1 diabetes. In order to exert their protolerogenic function, fibrocytic MDSCs require direct contact with activated T cells, which leads to the production and secretion of IDO. This new myeloid subset may have an important role in the in vitro and in vivo production of Treg cells for the treatment of autoimmune diseases, and in either the prevention or control of allograft rejection.
2014
44
3307-19
3319
Human fibrocytic myeloid-derived suppressor cells express IDO and promote tolerance via Treg-cell expansion / Zoso, Alessia; Mazza, Emilia Maria Cristina; Bicciato, Silvio; Mandruzzato, Susanna; Bronte, Vincenzo; Serafini, Paolo; Inverardi, Luca. - In: EUROPEAN JOURNAL OF IMMUNOLOGY. - ISSN 0014-2980. - ELETTRONICO. - 44:(2014), pp. 3307-19-3319. [10.1002/eji.201444522]
Zoso, Alessia; Mazza, Emilia Maria Cristina; Bicciato, Silvio; Mandruzzato, Susanna; Bronte, Vincenzo; Serafini, Paolo; Inverardi, Luca
File in questo prodotto:
File Dimensione Formato  
Zoso_et_al-2014-European_Journal_of_Immunology.pdf

Accesso riservato

Tipologia: Versione pubblicata dall'editore
Dimensione 1.46 MB
Formato Adobe PDF
1.46 MB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1061495
Citazioni
  • ???jsp.display-item.citation.pmc??? 60
  • Scopus 108
  • ???jsp.display-item.citation.isi??? 100
social impact