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

Hong Bin Ji, Gongxian Liao, William A. Faubion, Ana C. Abadía-Molina, Cristina Cozzo, F. Stephen Laroux, Andrew Caton, Cox Terhorst

Research output: Contribution to journalArticle

169 Scopus citations

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 languageEnglish (US)
Pages (from-to)5823-5827
Number of pages5
JournalJournal of Immunology
Volume172
Issue number10
DOIs
StatePublished - May 15 2004

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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