Conjunctivitis of allergic origin: immunologic mechanisms and current approaches to therapy.
The pathogenesis of ocular allergy involves multiple mechanisms, which lead to mast cell degranulation and the release of chemical mediators. Mast cell mediators that have been implicated in allergic ocular disease include histamine, eosinophil chemotactic factors, eosinophil granule major basic protein, platelet-activating factor, prostaglandin D2, and several other less well-defined preformed or newly synthesized mediators. The release of these chemical mediators ultimately results in conjunctival vasodilation, increased vascular permeability, leukocyte chemotaxis, and, rarely, ocular surface destruction. Current therapy of ocular allergy involves elimination of the offending allergen, modulation of the immune system, and pharmacologic inhibition of the chemical mediators. The purpose of this article is to provide a better understanding of the pathogenesis and current therapy of ocular allergic disorders and to review the central role of the mast cell and chemical mediators involved in ocular allergy.
Abelson
M B
MB
Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Schaefer
K
K
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D002634:Chemotaxis, Leukocyte; D003233:Conjunctivitis, Allergic / Q000188:drug therapy* / Q000276:immunology*; D005938:Glucocorticoids / Q000627:therapeutic use; D006634:Histamine H1 Antagonists / Q000627:therapeutic use; D006801:Humans
D000894:Anti-Inflammatory Agents, Non-Steroidal; D005938:Glucocorticoids; D006634:Histamine H1 Antagonists