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There are many studies dedicated to the allergic nose, but most of them deal with seasonal allergic rhinitis and particularly with acute experimental situations. Perennial allergic rhinitis is less well documented.
When studying the allergic nose, several aspects must be taken into consideration: the genetic background of the patient, various environmental factors (antigens, air pollution, climate), and the peculiar characteristics of the nose itself including its anatomy—total surface area: 150 cm2, volume: 15 ml—and histology—epithelium (ciliated, non ciliated, pseudostratified, columnar, goblet cells), mucus, immunocompetent cells, lamina propria, basement membrane, blood supply, and nerves and neurotransmitters.1
It is well recognised that the symptoms of perennial allergic rhinitis are caused by overproduction of different families of chemical mediators. These mediators are produced by migrating or resident inflammatory cells, by resident cells, or by inflammatory cells produced locally from progenitors—for example, T cells, mast cells, eosinophils, neutrophils, epithelial cells, endothelial cells, and antigen presenting cells (APCs). This review focuses on some recent aspects of perennial allergic rhinitis which cast new light on the pathophysiology of this common disease.
Cytokine profile in perennial allergic rhinitis
Since the description by Mosmann2 of the dichotomy of the murine T cell, a Th2/Th1 imbalance has been described in allergic conditions in humans. The nasal mucosa in perennial allergic rhinitis is characterised by the presence of a high percentage of activated Th2 cells accompanied by high levels of Th2 …
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