IgE responsiveness, atopic

Immediate hypersensitivity reaction - type I reaction, involves immunoglobulin E (IgE)-mediated release of chemical mediators from mast cells and basophils. Th2 cells produce IL-4 and IL-13, which then act on B cells to promote the production of antigen-specific IgE. Reexposure to the antigen can then result in the antigen binding to and cross-linking the bound IgE antibodies on the mast cells and basophils. This causes the release of preformed mediators (histamine, tryptase, tryptase, chemotactic factors), newly synthesized mediators (leukotrienes, prostaglandin, thromboxane, platelet-activating factor, adenosine, bradykinin), and cytokines from these cells that results in structural and functional changes to the affected tissue.

Also known as: IgE responsiveness, atopic, IgE, elevated level of, immediate hypersensitivity, type 1 hypersensitivity, type 1 hypersensitivity reaction, type I hypersensitivity, type I hypersensitivity reaction, type I immediate hypersensitivity reaction

17 clinical trials for this condition and its sub-types.