Peroxisome proliferator‐activated receptor (PPAR)‐γ is a nuclear hormone receptor that serves as a trans factor to regulate lipid metabolism. Intense interest is focused on PPAR‐γ and its ligands owing to its putative role in adipocyte differentiation. Little is known, however, about the functions of PPAR‐γ in the immune system, especially in T lymphocytes. We demonstrate that both naive and activated ovalbumin‐specific T cells from DO11.10‐transgenic mice express PPAR‐γ mRNA and protein. In order to determine the function of PPAR‐γ, T cells were stimulated withphorbol 12‐myristate 13‐acetate and ionomycin or antigen and antigen‐presenting cells. Simultaneous exposure to PPAR‐γ ligands (e. g. 15‐deoxy‐Δ^12, 14‐prostaglandin J₂, troglitazone) showed drastic inhibition of proliferation and significant decreases in cell viability. The decrease in cell viability was due to apoptosis of the T lymphocytes, and occurred only when cells were treated with PPAR‐γ, and not PPAR‐α agonists, revealing specificity of this response for PPAR‐γ. These observations suggest that PPAR‐γ agonists play an important role in regulating T cell‐mediated immune responses by inducing apoptosis. T cell death via PPAR‐γ ligation may act as a potent anti‐inflammatory signal in the immune system, and ligands could possibly be used to control disorders in which excessive inflammation occurs.