Dendritic cells (DCs) are crucial to shape the adaptive immune response. Extensive in vitro manipulation reprograms T H 2 and T H 17 cell lines into T H 1 cells, leading to the concept of CD4 + T H cell subset plasticity. The conversion of memory T H 17 cells into T H 2 cells or vice versa remains to be clarified.We examined the localization of T H 17/T H 2 cells in vivo, their cellular origin (T H 2 vs T H 17), and the underlying mechanisms that drive the generation of these double T H producers.Antigen-loaded bone marrow–derived DCs (ovalbumin-DCs) were repeatedly administered locally (intratracheally) or systemically (intravenously) to naive mice to elicit chronic airway inflammation. Inflamed lungs and mediastinal lymph nodes were examined for the presence of IL-17 + IL-13 + IL-4 + CD4 + T cells that coexpressed retinoic acid receptor–related orphan receptor γt and GATA-3 (T H 17/T H 2).We show that repetitive administration of inflammatory ovalbumin-DCs, locally or systemically, promoted the development of antigen-specific T H 17/T H 2 cells in lungs and mediastinal lymph nodes. Immunized mice had IgE-independent and steroid-resistant airway inflammation with a mixed neutrophil and eosinophil infiltration of the bronchoalveolar lavage fluid. Airway inflammatory signal regulatory protein α–positive DCs reprogrammed in vitro–generated T H 17 but not T H 2 cells, as well as lung effector T H cells, into T H 17/T H 2 cells.We demonstrate the existence of T H 17/T H 2 cells that express GATA-3 in inflamed tissues and their T H 17 origin. We further propose that repeated immunization with inflammatory DCs prevails on the route of DC administration to drive T H 17/T H 2-associated chronic lung inflammation.