Allergic asthma (AA) and allergic rhinitis (AR) are chronic allergic airway diseases characterised by a type 2 inflammatory response. Increased levels of type 2 cytokines (IL4, IL13, IL10 and IL5) cause a systemic increase in allergen reactive immunoglobulin (Ig) E levels. Next to these systemic effects, both in AA and AR, elevated levels of mucosal IgM, IgA, IgG and IgE antibodies have been described. Morover, the nasal and airway mucosa are enriched for antibody-secreting cells. The production of antibody-secreting cells has been classically attributed to secondary lymphoid organs (SLO), where distinct B cell follicles can be found enabling B cell selection and differentiation in response to antigen in germinal centers (GC). Yet, in AA and AR, tertiary lymphoid organs (TLO) are induced in the airway mucosa, which harbour local GC reactions. Whether TLO GC reactions effectively contribute to the generation of differentiated memory B cells, antibody-secreting cells and mucosal antibodies, is to date unclear. By studying TLO and mucosal immunoglobulins in allergic airway disease, we aim to elucidate the mechanisms driving mucosal B cell differentiation. These insights are important since local antibody production can modulate the severity of chronic allergic airway disease. Part from increasing our understanding of these basic immunological mechanisms, these insights can be important to optimise current allergen immunotherapy and vaccination strategies.