Basophils, together with mast cells, are the main effector cells in IgE-mediated allergic responses. Upon exposure to allergens, IgE antibodies bound to high-affinity IgE receptors (FcεRI) become cross-linked, leading to the release of mediators, including the chemokine CCL2, which is responsible for immune cell migration. The precise molecular mechanisms of communication via the chemokine CCL2 during an allergic reaction are unknown. In our study, we included patients with allergic reactions and healthy donors. From the blood of patients and healthy donors, we isolated basophils, which were used in in vitro studies. Mast cells derived from blood progenitor cells were passively sensitized and stimulated with allergen or anti-IgE. In mast cell supernatants, we measured the concentrations of nine cytokines known to influence immune cell chemotaxis (CCL2, CCL5, CCL11, MIP-1α, IL-8, IL-10, IL-13, GM-CSF, and VEGF). We then examined the effect of mast cell–derived CCL2 on basophil migration in vitro and its impact on endothelial monolayer permeability using human umbilical vein endothelial cells (HUVECs). Stimulation with allergen or anti-IgE induced significant release of CCL2, GM-CSF, IL-8, and VEGF from mast cells. Furthermore, overnight exposure to IL-33 enhanced the production of several cytokines. Mast cell–derived CCL2 not only increased basophil migration in vitro but also enhanced endothelial monolayer permeability in HUVECs. This effect was reduced by a CCR2 receptor antagonist, indicating the involvement of CCL2 signaling through the CCR2 receptor. In the future, the results of our research could potentially influence the development of biological drugs that could be administered to all patients at risk of developing acute allergic reactions, thereby no longer being limited to specific allergen immunotherapies.
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