Modèle BioRender

Novel Pathway of IgE-Mediated Drug Allergy

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Katja Martin

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BioRender Team

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Description: This template was adapted from the original submission. Edits were made to enhance scientific accuracy, optimal usability and/or to meet industry-leading design standards for science communication. Exposure and sensitization to certain drugs can ultimately lead to Ig-E mediated allergic reactions. ① Dendritic cells take up covalently bound happen-carrier adducts (true antigens), process them into peptides, then present them on HLA to T cells. ② T cells in response secrete cytokines to promote B-cell maturation into plasma cells that produce hapten-carrier-specific IgE. ③ Released IgEs bind to receptors on mast cells, where they cross-link to hapten-carrier complexes. Increasing amounts of hapten-carrier/IgE antibodies interaction with receptors make mast cells unresponsive. ④ Upon re-exposure, drugs can form large amounts of non-covalent drug-carrier complexes (fake antigens) that can bind to the preformed drug-specific IgE on mast cells, prompting mast cell degranulation, with clinical symptoms

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This template was adapted from the original submission. Edits were made to enhance scientific accuracy, optimal usability and/or to meet industry-leading design standards for science communication. Exposure and sensitization to certain drugs can ultimately lead to Ig-E mediated allergic reactions. ① Dendritic cells take up covalently bound happen-carrier adducts (true antigens), process them into peptides, then present them on HLA to T cells. ② T cells in response secrete cytokines to promote B-cell maturation into plasma cells that produce hapten-carrier-specific IgE. ③ Released IgEs bind to receptors on mast cells, where they cross-link to hapten-carrier complexes. Increasing amounts of hapten-carrier/IgE antibodies interaction with receptors make mast cells unresponsive. ④ Upon re-exposure, drugs can form large amounts of non-covalent drug-carrier complexes (fake antigens) that can bind to the preformed drug-specific IgE on mast cells, prompting mast cell degranulation, with clinical symptoms

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