GSE132699
The Effect of Steroid and ERa agonism on Th2 cells
Allergic asthma is a T helper 2 (Th2) cell-associated inflammatory disease, driven by cytokines such as IL-4, IL-5, and IL-13. Th2 cells express the G-protein-coupled receptor CRTh2, a receptor for prostaglandin D2 (PGD2) that influences Th2 function and survival. Inhaled glucocorticosteroids are the primary treatment of allergic asthma and improve asthma symptoms by inhibiting Th2 cytokine production. Women are more likely than men to have severe asthma and to have symptoms requiring a hospital visit. These findings lead us to consider a mechanism by which female sex hormones could influence Th2 cell response to glucocorticosteroid. Using whole-mRNA sequencing, we examined gene expression in primary Th2 cells following exposure to glucocorticosteroids (0.1µM) in the presence or absence of an estrogen mimic, PPT (10µM). Overall design: Gene expression in a primary Th2 cell line following treatment with Dexamethasone, PPT or both. Three replicates per condition, four conditions including control (Ethanol vehicle). 12 samples total.