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The Journal of Immunology, 2004, 172: 5823-5827.
Copyright © 2004 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: The Natural Ligand for Glucocorticoid-Induced TNF Receptor-Related Protein Abrogates Regulatory T Cell Suppression 1

Hong-bin Ji*, Gongxian Liao*, William A. Faubion*, Ana C. Abadía-Molina*, Cristina Cozzo{dagger}, F. Stephen Laroux*, Andrew Caton{dagger} and Cox Terhorst2,*

* Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215; and {dagger} Wistar Institute, Philadelphia, PA 19104

CD4+25+ regulatory T (Treg) cells maintain immunological self-tolerance through mechanisms that are only in part understood. Previous studies suggest that the glucocorticoid-induced TNFR-related protein (GITR), which is preferentially expressed on the surface of Treg cells, potentially provides a signal that abrogates Treg suppression. In this study, we show that a soluble form of mouse GITR ligand (sGITR-L) induces GITR-dependent NF-{kappa}B activation and blocks in vitro suppression mediated by both resting and preactivated polyclonal and Ag-specific Treg cells. Since sGITR-L along with rIL-2 induces proliferation of CD4+25+ cells, it appears that sGITR-L can break the anergic state of Treg cells. Because sGITR-L also up-regulates IL-2 secretion by activated CD4+25 –T cells, these two sGITR-L induced signals synergize to interfere with suppressor activity by CD4+25+ Treg cells.




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