Fig. 11.

CXCL11 robustly activates SRE and SRF response element signaling at CXCR3A, but not CXCR3B. HEK 293T cells were transiently transfected with either the SRE or SRF reporter and CXCR3A or CXCR3B. Prior to acquiring luminescence signal, cells were incubated for 5 hours with ligand (1 μM). CXCL11 incubation caused a significant increase in luminescence signal in both SRE-transfected (A) and SRF-transfected (C) cells. In cells transfected with CXCR3B, none of the endogenous ligands tested resulted in significant SRE (B) or SRF (D) signal, although cells still responded to the positive fetal bovine serum (FBS) control. In (E) and (F), cells were pretreated either with vehicle or with mitogen-activated protein kinase kinase (MEK) inhibitor PD98059 (20 μM). The CXCL11-induced SRE and SRF signals were sensitive to MEK inhibition (E and F); *P < 0.05. (A)–(D) One-way analysis of variance (ANOVA) and Tukey’s post hoc comparisons of treatment groups. The positive control of 10% FBS is included for reference, but not included in statistical analyses. (E) and (F) One-way ANOVA, followed by a directed Bonferroni post hoc comparison of vehicle (Veh) + CXCL11 to PD98059 + CXCL11, was conducted. n ≥ 3 biologic replicates per condition.