作者: Hong-bin Ji , Gongxian Liao , William A Faubion , Ana C Abadía-Molina , Cristina Cozzo
DOI: 10.4049/JIMMUNOL.172.10.5823
关键词:
摘要: CD4(+)25(+) regulatory T (Treg) cells maintain immunological self-tolerance through mechanisms that are only in part understood. Previous studies suggest the glucocorticoid-induced TNFR-related protein (GITR), which is preferentially expressed on surface of Treg cells, potentially provides a signal abrogates suppression. In this study, we show soluble form mouse GITR ligand (sGITR-L) induces GITR-dependent NF-kappaB activation and blocks vitro suppression mediated by both resting preactivated polyclonal Ag-specific cells. Since sGITR-L along with rIL-2 proliferation it appears can break anergic state Because also up-regulates IL-2 secretion activated CD4(+)25 (-)T these two induced signals synergize to interfere suppressor activity