2024/08/27 by Martin F. Bachmann, Pascal S. Krenger, Mona O. Mohsen +6
Immunology and Microbiology · Medicine · #Asthma and respiratory diseases #Mast cells and histamine #Monoclonal and Polyclonal Antibodies Research
paper · pdf · doi:10.1111/all.16248
openalex publication_date 2024/08/27 · openalex created_date 2024/08/28 · openalex updated_date 2026/07/28
Type I hypersensitivity, also known as classical allergy, is mediated via allergen-specific IgE antibodies bound to type I FcR (FcεRI) on the surface of mast cells and basophils upon cross-linking by allergens. This IgE-mediated cellular activation may be blocked by allergen-specific IgG through multiple mechanisms, including direct neutralization of the allergen or engagement of the inhibitory receptor FcγRIIb which blocks IgE signal transduction. In addition, co-engagement of FcεRI and FcγRIIb by IgE-IgG-allergen immune complexes causes down regulation of receptor-bound IgE, resulting in desensitization of the cells. Both, activation of FcεRI by allergen-specific IgE and engagement of FcγRIIb by allergen-specific IgG are driven by allergen-binding. Here we delineate the distinct roles of antibody affinity versus avidity in driving these processes and discuss the role of IgG subclasses in inhibiting basophil and mast cell activation.