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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: J Allergy Clin Immunol. 2019 Jun 24;144(2):381–392. doi: 10.1016/j.jaci.2019.06.010

FIGURE I: Key advances in mechanisms of allergy, urticaria and anaphylaxis in 12018.

FIGURE I:

Within mast cells, GATA 2 induced MITF, CRF2 downregulated IgE-mediated degranulation, and Stx 3 clustering on the plasma membrane induced mast cell exocytosis. Secreted exosomes (EX) also transfered FcεRI and bound to free IgE. Within basophils, SYK expression was modulated by anti-FcεR1. On epithelial cells, anaphylaxis depended on IL-4’s interaction with the VE-specific IL4Rα, and on binding of tropomyosin with dectin-1. Perivascular dendritic cells also captured blood-borne allergens (smallest green circles) and relayed them via MVs to neighboring mast cells and dendritic cells. In primed drug specific T cell clones and naïve T cells, high amounts of IL-22 were secreted, and in peripheral blood mononuclear cells, miRNA-9, miRNA-18a, miRNA21, and/or miRNA-155 were upregulated. MVs derived from activated T cells stimulated mast cell degranulation, in part by carrying miRNA-4443 (red rectangles). FcγRIIA-expressing platelets were activated by aggregated IgG and induced anaphylaxis.

Abbreviations: CRF: corticotropin releasing factor; CSU: Chronic spontaneous urticaria; EX-exosome; FcεRI: high affinity receptor for the Fc region of immunoglobulin E; IL4Rα: Receptor for interleukin 4; MiRNA: microRNA; MITF: microphthalmia-associated transcription factor; PLT: platelet; platelet; STX: syntaxin; SYK: spleen tyrosine kinase Th: T helper; VE: vascular endothelial