Fig. 6

Elevation of A_2AR signal in the CP epithelium increased the permeability and promoted the migration of T cells. A, B In the primary CP epithelium, the A_2AR agonist CGS21680 (100 nM, treatment for 2 h) increased the phosphorylation level of STAT3 (n = 3/group). C, D In the primary CP epithelium, the A_2AR agonist CGS21680 (100 nM, treatment for 2 h) also increased the phosphorylation level of p65 (n = 3/group). E Pre-treatment with NF-κB transcriptional activity inhibitor (JSH-23, 10 μM) or specific STAT3 inhibitor (Stattic, 100 μM) for 1 h abolished the increased expression of ccl20 induced by CGS21680 (100 nM, treatment for 2 h) in the primary CP epithelium (n = 4/group). F Representative image of ZsGreen-labeled A_2ARs overexpressed in the Z310 cell line. G Over-expression of A_2AR increased the resistance value of Z310 cells (n = 3/group). Unpaired t test. H, I Over-expression of A_2AR promoted the migration of CD4⁺ T cells across the Z310 cell layer (n = 3/group). Unpaired t test. J Following the addition of CGS21680 into the medium, the resistance values of the primary CP epithelium were monitored in real-time within 2 h (n = 3/group). One-way RM ANOVA, Dunnett’s multiple comparisons test. ^##p < 0.01, *p < 0.05 and **p < 0.01. “p” stands for phosphorylation