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Figure 1 | World Allergy Organization Journal

Figure 1

From: Eosinophils in Chronic Urticaria: Supporting or Leading Actors?

Figure 1

Immune mechanisms and main effector cells involved in chronic urticaria. A, Mast cells are activated either by autoantibodies to FeεRI or IgE and/or by other histamine releasing factors and release several mediators (histamine, leukotrienes, VEGF) that concur to produce the marked vasodilation that stands at the basis of both wheal-and flare reaction and angioedema. Some mediators and chemokines released by mast cells can recruit and activate eosinophils that in turn release inflammatory mediators and produce tissue factor, the main initiator of the extrinsic pathway of the coagulation cascade. The major basic protein released by eosinophils can induce mast cell degranulation. B, Eosinophils can be activated either directly by autoantibodies against the low affinity IgE receptor or indirectly by mast-cell derived mediators. C, Activated T-cells can induce mast cell degranulation by cell-to-cell contact. This process leads to the formation and release of cytokines such as TNF-α that has the capacity to induce gene expression in mast cells by an autocrine mechanism. ECP, eosinophil cationic protein; GM-CSF, granulocyte-monocyte colony-stimulating factor; MBP, major basic protein; PAF, platelet-activating factor; SCF, stem cell factor.

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