Instruction of Treg commitment in peripheral T cells is suited to reverse autoimmunity.
In order to exploit regulatory T cells in a clinical setting it is desirable to be able to generate such cells by a variety of antigens that elicit unwanted immune responses. This goal has been achieved by targeting antigen to dendritic cells under subimmunogenic conditions which results in the conversion of naïve Foxp3 negative T cells into Foxp3-expressing regulatory T cells that are indistinguishable from what has been referred to as natural Treg. Such cells have the ability to interfere with immunity at early as well as late stages of the immune response during which effector cells have already been formed. This suggests that Treg cannot only be exploited to prevent immune responses but also to interfere with already established immunity.
Harvard Medical School, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA.
Elmar
E
Jaeckel
Karsten
K
Kretschmer
Irina
I
Apostolou
Harald
H
von Boehmer
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology* / Q000628:therapy*; D002454:Cell Differentiation / Q000276:immunology*; D006801:Humans; D050378:T-Lymphocytes, Regulatory / Q000166:cytology* / Q000276:immunology*