Novel approaches in the inhibition of IgE-induced mast cell reactivity in food allergy

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Allergy is an IgE-dependent type-I hypersensitivity reaction that can lead to life-threatening systemic symptoms such as
anaphylaxis. In the pathogenesis of the allergic response, the common upstream event is the binding of allergens to specific IgE,
inducing cross‐linking of the high‐affinity Fc􀀀RI on mast cells, triggering cellular degranulation and the release of histamine,
proteases, lipids mediators, cytokines and chemokines with inflammatory activity. A number of novel therapeutic options to curb
mast cell activation are in the pipeline for the treatment of severe allergies. In addition to anti-IgE therapy and allergen-specific
immunotherapy, monoclonal antibodies targeted against several key Th2/alarmin cytokines (i.e. IL‐4Rα, IL‐33, TSLP), active
modification of allergen-specific IgE (i.e. inhibitory compounds, monoclonal antibodies, de-sialylation), engagement of inhibitory
receptors on mast cells and allergen-specific adjuvant vaccines, are new promising options to inhibit the uncontrolled release of
mast cell mediators upon allergen exposure. In this review, we critically discuss the novel approaches targeting mast cells limiting
allergic responses and the immunological mechanisms involved, with special interest on food allergy treatment.

Bibliographical metadata

Original languageEnglish
JournalFrontiers in Immunology
Publication statusPublished - 2021