Fine control of immune cell activation is critical for preventing inflammatory disease, particularly in barrier sites such as the lung. However, the central mechanisms involved in controlling pulmonary macrophages and dendritic cells (DCs) during type-2 inflammation are currently poorly understood. We have found that the lung environment dramatically impairs the ability of alveolar macrophages to respond during type-2 inflammation following administration of IL-4 complex (IL-4c), allergen exposure or helminth infection, and identified which DC subpopulations are associated with induction of type-2 outcomes in such settings. Together, our data provide novel insight into the fundamental mechanisms that control macrophage and DC activation and function during pulmonary type-2 inflammation.