Food Allergy Pathogenesis


Pathophysiological Mechanisms of Allergic

The pathophysiological mechanisms of allergy own immediate hypersensitivity reactions of type I, which is the most serious clinical manifestation of anaphylaxis occur both as local and systemic reactions. The systemic reaction generally follows the intravenous administration of an antigen previously used in which the host has been previously sensitized, this leads to a state of shock, even fatal.

The local nature of the reaction varies depending on the input port of the antigen, it may take the form of a localized skin edema (allergic rash or hives ); nasal discharge and conjunctivitis ( allergic rhinitis and allergic conjunctivitis), hay fever or asthma and Gastrointestinal events (vomiting, diarrhea, abdominal pain).

The type I hypersensitivity reactions occur in two phases:

1. immediate phase
sensitization phase (first exposure to antigen)
phase tripping

2. being delayed or secondary
The mast cell (see picture) has a crucial role in the development of disease . It is anatomically placed in strategic areas for the immune response, such as blood vessels , the mucous membrane , the nerve . The mast cell activation occurs through a link between the receptors and IgE. Another important step in the process of cellular immediate hypersensitivity type I cells is determined by the Th2 : they receive the signal from the antigen-presenting cells ( macrophages and dendritic cells ), after which the Th2 differ and produce different cytokines ; the latter are used to activate the production of IgE by B cells (sensitization phase). Mast cells together with basophils express membrane receptors FcεR, with high affinity for IgE. When mast cells are coated with IgE on the surface after an initial sensitization phase, the subsequent contact with the antigen determines the relationship between 2 molecules of IgE and the receptor FcεR. This link (antigen + 2 IgE + receptor FcεR) determine an activation of the transduction signal cytoplasmic of mast cell Ca + + dependent, involving the fusion of vesicles lysosomal full of mediators , especially histamine , with the inner surface of the membrane of mast cell and subsequent release of chemical mediators stored (step tripping). These mediators are responsible for the symptoms of Type I hypersensitivity reactions both localized and systemic responses also active late-type.

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