One key co-stimulatory molecule present on the surface of DCs—glucocorticoid-induced tumor necrosis factor receptor ligand (GITRL)—via binding to its corresponding T-cell ligand GITR serves to inhibit Treg-mediated Th cell suppression and enhance Th2 cell activity, thus augmenting AHR, serum IgE levels, and Th2 cytokine release in a murine model of asthma (16). The gene discussed is TNFSF18; the disease is asthma.