[Pathophysiology of chronic allergic rhinitis]. / Patofizjologia przewleklych, alergicznych niezytów nosa.

ABSTRACT

The last ten or fifteen years have provided truly novel insight into the molecular and cellular pathobiology of allergic diseases. Whether cytokine regulation of mast cells is autocrine in part or entirely the purview of the T cell, remains to be determined, but still emphasizes the complex cellular interaction in sustained reactions falling within the clinical definition of allergy. The rapid advances being made in understanding the biochemistry and function of the three categories of adhesion molecule involved in allergic reaction. Cell adhesion molecules are glycoproteins, identified within the last decade, expressed on all surfaces that allow cell-to-cell contact, control immune surveillance and effector functions. The three families of adhesion molecules that participate in this vital processes are the selectins, namely L-selectin, E-selectin and P-selectin, the integrins LFA-1, CR-3, p 150.95 and very late antigen 4, and the immunoglobulin (Ig) superfamily which includes intercellular adhesion molecule 1 (ICAM-1), ICAM-2 and vascular cell adhesion molecule 1 (VCAM-1). These adhesion molecules play an essential role in the pathogenesis of allergic rhinitis.