Regulatory T (T_reg) cells control immune activation and maintain tolerance. How T_regs mediate their suppressive function is unclear. Here we identified a cell surface molecule, called GARP, (or LRRC32), which within T cells is specifically expressed in T_regs activated through the T cell receptor (TCR). Ectopic expression of GARP in human naïve T (T_N) cells inhibited their proliferation and cytokine secretion upon TCR activation. Remarkably, GARP over-expression in T_N cells induced expression of T_reg master transcription factor Foxp3 and endowed them with a partial suppressive function. The extracellular but not the cytoplasmic region of GARP, was necessary for these functions. Silencing Foxp3 in human T_reg cells reduced expression of GARP and attenuated their suppressive function. However, GARP function was not affected when Foxp3 was downregulated in GARP-overexpressing cells, while silencing GARP in Foxp3-overexpressing cells reduced their suppressive activity. These findings reveal a novel cell surface molecule-mediated regulatory mechanism, with implications for modulating aberrant immune responses.