In: Biology
Type I Hypersensitivity is mediated by the antibody class named IgE. When an allergen is encountered by the immune system, the allergen-specific IgE antibodies that are present in innate immune-system cells like mast cells, basophils, and eosinophils, they crosslink the Fc receptors of those cells. Crosslinking of Fc receptors that specifically bind IgE antibodies produces a response called degranulation. The granules stored in the innate immunity cells are released by degranulation. Degranulation release mediators such as histamine, leukotrienes, prostaglandin, etc. that function to produce physiological symptoms of hypersensitivity such as increased vascular permeability, contraction of smooth muscles, excess mucosal activity, and platelet aggregation.
The first exposure to an allergen often does not result in acute inflammation. This is because the allergen-specific IgE is not made yet. Normally, antibodies are produced in response to a pathogenic determinant only when it is recognized by a B-cell having a membrane-bound immunoglobulin capable of recognizing the determinant. Once an antibody is produced against a pathogenic molecule, it is recognized quickly when the molecule is encountered again in the future. In the case of allergy, instead of a pathogen, an environmental determinant is mistaken as a pathogenic determinant upon its first exposure. Consequently, the allergen-specific IgE is produced so that at the time of later exposure the antibody can bind to the allergen quickly.