The anaphylatoxin C5a plays an important role during the development of maladaptive Th2 and Th17 responses in allergic asthma. Recently we identified a new anti-inflammatory mechanism, by which IgG1 immune complexes (IC) block C5a-mediated effector functions in vitro and in vivo in mouse models of inflammation. Galactosylation of the IgG Fc part is essential for this effect. In this project, we aim at delineating the regulatory effects of highly galactosylated IgG1 IC  on the development of allergic asthma. For this purpose, we will assess the impact of highly galactosylated IgG1 IC on the development of house dust mite (HDM)-induced experimental allergic asthma during allergen sensitization and in established disease.