Abstract
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-κB 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.
Original language | English (US) |
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Pages (from-to) | 5823-5827 |
Number of pages | 5 |
Journal | Journal of Immunology |
Volume | 172 |
Issue number | 10 |
DOIs | |
State | Published - May 15 2004 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology