phaidra.vetmeduni.ac.at o:5627 DOI 10.1111/all.70229 Allergic Sensitization to Inhalant Allergens in the Upper Respiratory Tract—the B Cell Side Allergic diseases are on the rise worldwide, driven by respiratory epithelial barrier dysfunction that promotes sensitization to inhalant allergens such as pollen, dust mites, pet dander, and fungal spores. These antigens trigger IgE-mediated immune responses that lead to diseases such as allergic rhinitis (AR) and asthma. B cells play a central role by producing allergen-specific IgE, presenting antigens, releasing cytokines, and forming memory B cells (MBCs). Their differentiation into IgE-secreting plasma cells (PCs) mainly relies on T cell help, germinal center (GC) reactions, and/or extrafollicular responses and class switch recombination (CSR), which makes them important therapeutic targets. The nasal mucosa, as the first point of contact for allergens, acts both as a barrier and as an immunological site. In AR, IL-13-driven goblet cell hyperplasia and overproduction of mucus compromise the integrity of the barrier. Although the nasal microbiome can influence the immune response, its role in atopy remains unclear. Local B cell activity, including extrafollicular IgE production and ectopic GCs, enhances mucosal immunity. Epithelial cells detect allergens via pattern recognition receptors (PRRs) and release alarmins (IL-25, IL-33, TSLP), which can trigger type 2 inflammation. Proteases from allergens such as house dust mites (HDM) disrupt epithelial junctions, while pollutants, smoke, microplastics, and allergen-derived metabolites further modulate immune activation. Allergens are transported to the lymph nodes by the passive flow to follicular dendritic cells (FDCs) or by active uptake by interferon regulatory factor (IRF) 4-dependent conventional type 2 DCs, which activate T follicular helper (TFH) cells to drive IgE responses. Advanced lymphoid organoids that mimic the microenvironment of GCs offer promising models for the study of allergic sensitization but require improved standardization. eng allergen transport B cells epithelial barrier IgE plasma cells nasal mucosa organoids 2026-10-22T08:26:06.647Z LOMv1.0 Author BEGIN:VCARD VERSION:3.0 N:Grimsholm;Ola; FN:Ola Grimsholm X-ORCID:https://orcid.org/0000-0003-2064-2556 END:VCARD BEGIN:VCARD VERSION:3.0 N:Zghaebi;Mohammed; FN:Mohammed Zghaebi X-ORCID:https://orcid.org/0000-0002-7636-2601 END:VCARD BEGIN:VCARD VERSION:3.0 N:Hambrecht;Bita; FN:Bita Hambrecht X-ORCID:https://orcid.org/0009-0005-7908-2305 END:VCARD BEGIN:VCARD VERSION:3.0 N:Kalic;Tanja; FN:Tanja Kalic X-ORCID:https://orcid.org/0000-0002-9641-0244 END:VCARD BEGIN:VCARD VERSION:3.0 N:Udoye;Christopher C.; FN:Christopher C. Udoye X-ORCID:https://orcid.org/0000-0001-8012-6217 END:VCARD BEGIN:VCARD VERSION:3.0 N:Manz;Rudolf; FN:Rudolf Manz X-ORCID:https://orcid.org/0000-0003-1263-7693 END:VCARD BEGIN:VCARD VERSION:3.0 N:Bohle;Barbara; FN:Barbara Bohle X-ORCID:https://orcid.org/0000-0002-5105-7985 END:VCARD BEGIN:VCARD VERSION:3.0 N:Sitnik;Katarzyna M.; FN:Katarzyna M. Sitnik X-ORCID:https://orcid.org/0000-0002-6965-0322 END:VCARD BEGIN:VCARD VERSION:3.0 N:Eckl‐Dorna;Julia; FN:Julia Eckl‐Dorna X-ORCID:https://orcid.org/0000-0001-5981-1607 END:VCARD BEGIN:VCARD VERSION:3.0 N:Breiteneder;Heimo; FN:Heimo Breiteneder X-ORCID:https://orcid.org/0000-0003-2022-8689 END:VCARD https://w3id.org/kim/hcrt/scheme https://w3id.org/kim/hcrt/text Textdokument Text LOMv1.0 yes https://creativecommons.org/licenses/by/4.0 application/pdf 1504590 https://phaidra.vetmeduni.ac.at/o:5627 https://phaidra.vetmeduni.ac.at/api/object/o:5627/thumbnail LOMv1.0 discipline