Mechanisms of allergen immunotherapy (IMAGE)
Caption
Natural low-dose allergen exposure on damaged airway epithelium promotes DC and ILC2, which induce Th2 and Tfh cell responses and release of type 2 cytokines. B cells undergo isotype switching to IgE-producing plasma cells and produce IgE under the regulation of type 2 cytokines. Tfh cells induce the development of Bmem through IL-4, IL-9, IL-21, and CD40 ligand–CD40 interaction. cTfh could share properties of memory cells. Allergen–IgE cross-linking of FcεRI receptors on MCs and basophils promotes release of granule-derived mediators such as histamine, tryptase, prostaglandin, leukotrienes and platelet activating factor. AIT induces the generation of DCreg, which stimulates ILC2 transformation to ILCreg and IL10+ ILCs, shift toward Th1 cell response, and Treg proliferation. IL-10, IL-35, and TGF-β secreted by Treg promote the differentiation of Breg cells and IgG/A-producing plasma cells. Tfr cells are a subset of CXCR5+ Foxp3+ Tregs, which downregulate Tfh cell-mediated type 2 immune response. Cytokines (e.g., IL-10, IL-35, IFN-γ, CTLA-4) secreted by ILCreg, IL10+ ILCs, Treg, Breg, Th1 cells, and Tfr inhibit Th2-type responses. IgG1/4 and IgA1/2 competitively inhibit allergen–IgE cross-linking to FcεRI on MCs and basophils, and IgE-facilitated antigen presentation and type 2 cell responses.
Credit
Dr. Yadong Gao from Philipps University of Marburg, Germany
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CC BY-NC-ND