Allergic asthma is a disease of the airways driven by maladaptive T helper 2 (Th2) and Th17 immune response against harmless, airborne substances. The hallmarks of this disease are airway hyperresponsiveness (AHR), eosinophilic and neutrophilic airway inflammation and mucus overproduction. Distinct dendric cell (DC) subsets together with airway epithelial and pulmonary vascular endothelial cells play critical roles in allergen sensing and in driving T cell differentiation towards Th2 and Th17 effector or regulatory T cells (Treg). Previous studies suggested already a pivotal role for the anaphylatoxins (C5a, C3a) in the pathogenesis of allergic asthma. During sensitization for example it is described, that C3a promotes, whereas C5a protects from the development of maladaptive immunity during allergen sensitization. Here we will discuss the role of the anaphylatoxins (C3a, C5a) and their receptors during the pathogenesis of allergic asthma, and specifically in lung DC biology. We will also have a look on canonical and non-canonical complement activation and we will discuss novel concepts on how the adaptive immune system can regulate the function of ATRs also in the context of allergic asthma.