A2AR<sup>-/-</sup> γδ T cells were unable to suppress Foxp3<sup>+</sup> T cell response.

<p>A) CD3<sup>+</sup> responder T cells isolated from immunized TCR-δ<sup>-/-</sup> mice were cultured with 1 ng/ml recombinant IL-2 in the presence or absence of γδ T cells isolated from immunized B6 or A2AR<sup>-/-</sup> mice and subsequently stained with a PE-labeled anti-Foxp3 antibody. B) Pretreatment of A2AR<sup>+/+</sup> γδ T cells with an A2AR antagonist (SCH 58261) abolished the enhancing effects. CD3<sup>+</sup> responder T cells isolated from immunized TCR-δ<sup>-/-</sup> mice were cultured with 1 ng/ml recombinant IL-2 for 5 days, in the absence (left panel) or presence (middle and right panels) of γδ T cells that were treated (right panel) or untreated with an A2AR antagonist. Foxp3<sup>+</sup> T cells in the cultures were identified. C) Blockade of high-affinity IL-2 receptor CD25 by monoclonal antibody (PC61) did not affect the inhibiting effect of γδ T cells. CD3<sup>+</sup> responder T cells isolated from immunized TCR-δ<sup>-/-</sup> mice were cultured with 1 ng/ml recombinant IL-2 for 5 days, in the absence (left panel) or presence (three right panels) of activated γδ T cells that were treated as indicated.</p>