P03 (2026 - 2030) Imprint of diet on B cell functions and IgE formation in atopic dermatitis

Katja Bieber (UzL), Ralf J. Ludwig (UzL)

Project Summary 

Atopic dermatitis (AD) is a common chronic idiopathic inflammatory skin disorder. It belongs to the spectrum of type 2 inflammatory diseases. Early onset and severe AD are significant risk factors for the development of food allergy and other type 2 inflammatory diseases, linking this projects to other projects of GRK 3095 addressing various aspects of food allergy. IgE-related immune responses, e.g., elevated levels of total serum IgE, are one mutual hallmark of type 2 inflammatory diseases. These include antibodies reactive to environmental allergens and/or self-proteins. However, the role of IgE in AD is not fully understood, potentially due to the existence of distinct AD endotypes, e.g. extrinsic and intrinsic AD. In line, the anti-IgE antibody omalizumab has shown varying results in the treatment of AD. IgE may contribute to AD through activation of innate effector cells. Alternatively, it has been postulated that CD23+ B cells capture IgE-allergen complexes to increase the AD allergen-specific T cell response and to contribute to epitope spreading. This project will investigate whether the skin driven immune reaction in AD yields IgE with comparable affinity to that in other atopic diseases such as food allergy and will address the mechanisms by which IgE could contribute to AD pathogenesis.