Journal of Immunology Research / 2016 / Article / Fig 2

Review Article

IgE-Related Chronic Diseases and Anti-IgE-Based Treatments

Figure 2

Pathophysiology of urticaria. In CSU patients, stimulation of mast cells (MC) and basophils (BS) can be triggered by IgE against autoantigens, by IgG against FcεRI or IgE against IgE itself, or by complement. Moreover, MC and BS can be stimulated by molecules secreted by other immune cells or neurons. Once activated, MC and BS secrete several preformed mediators, such as histamine or tryptase, and other de novo mediators, such as prostaglandins and leukotrienes, will promote inflammation, vascular permeability, and vasodilatation, as well as neuron stimulation. These effects are transduced into edema and pruritus. Secretion of cytokines by MC and BS triggers migration of other immune cells to the skin, which will contribute to skin inflammation. MBP: major basic protein; NFG: nerve growth factor; PAF: platelet-activating factor; NO: nitric oxide.

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