This mechanism allows cells producing IL‐4 and IL‐13 to further enhance Th2 cell polarization in response to allergens.[116] Moreover, the interaction of IL‐4 and IL‐13 with allergens or TLR agonists stimulates lung epithelial cells to produce TSLP, GM‐CSF, and the chemokine CCL20.[117] Thus, effector cells of asthma may maintain Th2 cell‐mediated inflammation directly, through the activation and recruitment of DCs, or indirectly, through the regulation of cross‐talk between epithelial cells and DCs.[112b]. The gene discussed is IL13; the disease is asthma.