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UCLA School of Medicine, Harbor-UCLA Medical Center, Bldg. N-25, 1000 W. Carson Street, Torrance, CA 90509, USA.
Mast cells not only function as effector cells but also influence nearly every other cell involved in causing allergic rhinitis. Mast cell-derived mediators such as histamine, bradykinin, tryptase, and the arachidonic acid derivatives produce the symptoms of the early-phase reaction of allergic rhinitis and also attract and activate other leukocytes involved in the late-phase reaction. In addition, activated mast cells are known to secrete a number of cytokines, both preformed and newly synthesized, that can modulate T- and B-cell function, propagate the early- and late-phase reactions, and contribute to tissue remodeling. Most currently available therapies work by antagonizing the mediators secreted by mast cells and other leukocytes. With the possible exception of immunotherapy, these therapies do not provide long-term protection against allergic disorders. Exciting new developments in gene-based therapies seem promising in both reducing and reversing the development of allergic rhinitis.
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