A2AR dysfunction compromised γδ T cells’ activation threshold.

<p>A) Failure to express A2AR rendered γδ T cells less activated. In a 24-well plate, 2 x 10⁵ A2AR^+/+ or A2AR^-/- γδ T cells were incubated with medium only (Control), with pooled cytokines (IL-1, IL-7, and IL-23), and with or without or NECA (300 nM) or the A2AR-specific agonist CGS21680. At 48 h after the culture, IL-17 amounts in the culture supernatants were assessed by ELISA. B) Blockade of A2AR expression prevented γδ T cell activation. Surface staining for the T cell activation marker CD25 showing that A2AR antagonist treated A2AR^+/+ γδ T cells express low amounts of CD25 after exposure to cytokines. The results shown are from a single experiment and are representative of those obtained in >5 experiments. **_, p < 0.01.