Allergy and Clinical Immunology

Hay fever, also known as allergic rhinitis, is an improper immune response to the introduction of an allergen such as pollen, mold or animal dander into the body. Allergic responses are an interaction between three factors; the allergen, mast cells and immunoglobulin E (IgE). Mast cells are found in connective tissues including the skin, mucosal lining of the nose, intestinal tract, upper airways and lungs and their surface is coated with IgE. Typical of other types of allergic reactions, hay fever consists of an acute and late phase response.

In the acute phase, allergen introduction stimulates the immune system to release significant quantities of IgE. IgE binds with high affinity to FC epsilon R1 receptors on the surface of both mast cells and basophils, inducing their degranulation. Products of degranulation include histamine, tryptase, chymase and other chemical mediators including cytokines, interleukins, leukotrienes and prostaglandins. Mast cells also secrete several inflammatory mediators de novo, including prostaglandin D2 and the sulfidopeptidyl leukotrienes (LT)C4, LTD4 and LTE4.

These mediators cause blood vessel leakage, inducing mucosal edema and watery rhinorrhea. Blood vessel dilation causes sinusoidal filling and congestion of nasal passages. These responses occur within minutes and are termed an acute allergic response (Skoner, 2001). In the late phase, acutely-released mast cell-derived mediators released now act on post-capillary endothelial cells to promote the expression of vascular cell adhesion molecule and E-selectin, both of which facilitate adhesion of leukocytes to the endothelial cells.

Secreted mast cell cytokines act as chemoattractants which induce migration of leukocytes to the mucosa. Mast cell secretions in the four to eight hours after an acute allergic response reactivate many of the pro-inflammatory reactions of the immediate response causing the persistent symptoms of hay fever.

WORKS CITED

Skoner, D. P. (2001). Allergic rhinitis: definition, epidemiology, pathophysiology, detection and diagnosis. Journal of Allergy and Clinical Immunology, 108(Supplement 1), S2-8.

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