Type I hypersensitivity (Allergy)

Antibodies belonging to IgE class mediate this type of hypersensitivity; antigens that induce them are called allergens. IgE antibodies bind to Fc receptors on mast cells and basophils. When these cell-associated antibodies are cross-linked by allergens, the cells are activated and release a variety of mediators. They cause increased vascular permeability, vasodilatation, bronchial and visceral smooth muscle contraction, and local inflammation.
Allergy comprises two similar, however clinically different, conditions, anaphylaxis and atopy, respectively. Anaphylaxis is the extreme and systemic form of the allergic reaction. Mast cell- or basophil-derived mediators can restrict airways to the point of asphyxation and produce cardiovascular collapse leading to death; each human being can suffer from. Atopy is mostly a localised IgE-mediated hypersensitivity reaction, which develops in the individuals only who are genetically predisposed to produce IgE antibodies in response to various environmental antigens. In addition to immediate reaction after allergen entry, atopy is characterised by a late phase reaction. It is mediated by an inflammatory infiltrate of eosinophils, basophils, neutrophils, and TH2 lymphocytes. It ensues 4 to 6 hours after mast cell and basophil degranulate. Repeated bouts of this late phase reaction are responsible for tissue damage. To atopic diseases belong urticaria, hay fever, asthma, and atopic eczema. Their treatment is based on a neutralisation of histamine, leucotrienes, IgE antibodies and suppression of ongoing inflammatory reactions by glucocorticoids.

Courses

• Immunology [020]

Related contributions:

• Antibodies. B cells
• Cytokines. PAMPs and PRRs