VMC 221: Veterinary Immunology and Serology (1+1)

MECHANISM

• An allergen induces a humoral antibody response and leads to formation of IgE from plasma cells.
• This IgE binds with high affinity Fc receptors on surface of tissue mast cells and basophils.
• Mast cells and basophils coated by IgE are said to be sensitized.
• A later exposure to the same allergen cross links the membrane bound IgE on sensitised mast cells and basophils causing degranulation of these cells.
• The combination of IgE with antigen on the surface of mast cells also provokes the formation of vasoactive molecules.
• It is these agents both released preformed from the granules and those newly synthesized that generate the characteristic lesions of Type I hypersensitivity.
• Mast cell granules contain histamine and in some species serotonin. Histamine causes smooth muscle contraction in the bronchi, GI tract, uterus and bladder.
• It increases vascular permeability causing fluid accumulation leading to wheal formation. It stimulates mucus secretion, lacrimation and salivation.
• Serotonin causes vasoconstriction resulting in the rise in blood pressure. In rats and mice it induces wheal and flare reaction.
• Trypsin or chymotrypsin like neutral proteases released can destroy nearby cells and activate the complement C3 and C5 to generate anaphylatoxins.
• Activation of the cycloxygenase pathway and lipoxygenase pathway lead to formation of prostaglandins and leukotrienes respectively (LTC4, LTD4 and LTE4 together were formerly called as slow reacting substances of anaphylaxis or SRS-A).
• Mast cell granules release eosinophil chemotactic factor – A (ECF-A) which accounts for eosinophilia characteristic of Type I hypersensitivity including helminthic infection.
• Various cytokines and heparin are also released due to degranulation. Due to release of heparin, blood from animals experiencing anaphylaxis and dogs with mast cell tumors fail to coagulate.

Click here...