Allergic conjunctivitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
The ocular allergic response is a cascade of events that is coordinated by mast cells.[1] Beta chemokines such as eotaxin and MIP-1 alpha have been implicated in the priming and activation of mast cells in the ocular surface. When a particular allergen is present, sensitization takes place and prepares the system to launch an antigen specific response. TH2 differentiatedT cells release cytokines, which promote the production of antigen specific immunoglobulin E (IgE). IgE then binds to IgE receptors on the surface of mast cells. Then, mast cells release histamine, which then leads to the release of cytokines, prostaglandins, and platelet-activating factor. Mast cell intermediaries cause an allergic inflammation and symptoms through the activation of inflammatory cells.[2]
When histamine is released from mast cells, it binds to H1 receptors on nerve endings and causes the ocular symptom of itching. Histamine also binds to H1 and H2 receptors of the conjunctival vasculature and causes vasodilatation. Mast cell-derived cytokines such as chemokine interleukin IL-8 are involved in recruitment of neutrophils. TH2 cytokines such as IL-5 recruit eosinophils and IL-4, IL-6, and IL-13, which promote increased sensitivity. Immediate symptoms are due to the molecular cascade. Encountering the allergen a patient is sensitive to leads to increased sensitation of the system and more powerful reactions. Advanced cases can progress to a state of chronic allergic inflammation.
References
- ↑ Liu G, Keane-Myers A, Miyazaki D, Tai A, Ono SJ (1999). "Molecular and cellular aspects of allergic conjunctivitis". Chem. Immunol. Chemical Immunology and Allergy. 73: 39–58. doi:10.1159/000058748. ISBN 3-8055-6893-2. PMID 10590573.
- ↑