“…However, not all patients with AERD can be desensitized, and this group that fails desensitization is distinguished by their constitutive overproduction and aspirin-stimulated release of PGD 2 that correlates with the severity of airflow obstruction 6 . In addition to defining a more severe subgroup that fails aspirin desensitization, PGD 2 likely contributes to the severity through its myriad of biological activities that includes inducing vasodilation and vascular leakage, bronchoconstriction, and the recruitment and activation of basophils, eosinophils, dendritic cells, and both Th2-like lymphocytes and type 2 innate lymphoid cells [8][9][10][11] .…”