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Abstract

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adhesion molecule)°¡ ¹éÇ÷±¸°¡ Ç÷°ü º®¿¡ Á¢ÂøÇÏ´Â °úÁ¤¿¡¼­ Áß¿äÇÑ ¿ªÇÒÀ» ÇÒ °ÍÀ̶ó´Â
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The late phase reaction in allergic rhinitis is now considered to be responsible for the
chronic nasal obstruction in the patients with allergic rhinitis. The main pathophysiology
of the late phase reaction comprises an accumulation of Inflammatory cells including
eosinophils and T-lymphocytes. How these cells are preferentially recruited remains
incompletely defined. Along with mast cells and other cells, they release a wide variety
of mediators, cytokines, and granule constituents that can directly cause inflammation or
activate local vascular endothelium to further enhance the recruitment of leukocytes
through the expression and the function of adhesion molecules.
Cell adhesion molecules are now known to be critical for virtually every step in cell
recruitment, Including margination, transendothelial migration, chemotaxis, and
transepithelial migration.
Cytokines can promote cell recruitment by altering the function and/or the expression
of leukocyte, endothelial, and/or epithelial cell adhesion molecules. While the
understanding of the importance of leukocyets and endothelial adhesion molecules is still
at a very early stage, recent evidence has already begun to implicate these cell surface
molecules in the pathogenesis of allergic diseases such as allergic rhinitis and asthma.

Å°¿öµå

Allergic rhinitis; Adhesion molecule; Eosinophil Pathophysiology Nasal polyp.;

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KAMS