Although a very prevalent disease, the exact pathogenesis of asthma remains incompletely understood. The inflammation seen in patients with asthma is analogous to those seen in chronic rhinosinusitis with nasal polyps. Both disorders occur often together in the same patient and share a T helper 2-biased, IL-13-mediated eosinophilic inflammation. We believe that chitin (present in house dust mite, in the fungal cell wall…), chitin degrading enzymes (chitinases) and chitinase like proteins play an important role in the immune response seen in type 2 inflammatory airway diseases. Further, we assume that the expression of chitinases is regulated by IL-13 and that anti-IL4-Ralpha/IL-13-Ralpha monoclonal antibodies (Dupilumab) might influence the chitinase expression and the chitinase induced effects. With this project, we aim to elucidate the regulation and the functions of chitinases and chitinase like proteins in type 2 inflammatory airway diseases.