Fig. 1.

BP patients demonstrated elevated serum levels of IgE and eosinophilia. Anti-BP180 IgE can bind to the FcεRI receptors in mast cells, leading to a crosslink with hemidesmosome, degranulation of mast cells and histamine release, amplifying the chemotaxis of eosinophils and neutrophils. Omalizumab is a monoclonal antibody against the Cε3 domain of IgE, blocking its interaction with the specific FcεRI receptor, leading to a reduction of total IgE levels and eosinophilia. IL-5 is a Th2 cell-induced cytokine that contributes to eosinophilic maturation, activation and chemotactic activity. Reslizumab and mepolizumab are both monoclonal antibodies that target IL-5. Benralizumab, a monoclonal antibody against IL-5RA, can cause direct apoptosis of eosinophils and basophils. IL-17 also enhances eosinophilia. Secukinumab and ixekizumab both target IL-17A. IL-23 is an important cytokine in IgE-mediated responses, which promotes and maintains IL-17 activity and therefore eosinophilia. Tildrakizumab targets IL-23. Ustekinumab is an IL-12 and IL-23 inhibitor (targets their common p40 subunit). BP bullous pemphigoid, IL interleukin, IL-5RA alpha subunit of the IL-5 receptor, IgE immunoglobulin E autoantibodies targeting hemidesmosomal protein BP180 (collagen XVII), Th2 type 2 helper