OBJECTIVE: Recent pathophysiologic research demonstrated the crucial role played by adhesion molecules in recruiting and activating inflammatory cells during allergic reaction. DATA SOURCES: Intracellular adhesion molecule (ICAM-1) expression on nasal epithelial cells is involved in two main pathogenetic phenomena. The first is to allow leukocyte infiltration of respiratory mucosa, since they express LFA1 and Mac1, which are ligands of ICAM-1. This point is very important, because it has been demonstrated that patients with mite allergy (ie, continuously exposed to allergen) present a minimal persistent inflammation (MPI) both at nasal and conjunctival levels. This inflammation is characterized by the presence of leukocyte infiltration and ICAM-1 expression on epithelial cells and by a relationship between specific and nonspecific hyperreactivity in the absence of clinical symptoms. The second is that ICAM-1 is also the main receptor of the human rhinoviruses. This fact may partially explain the relationship among allergy, viral infections, and asthma attacks. STUDY SELECTION: Different studies have been performed to demonstrate the possible effects on the different clinical aspects of MPI exerted by an antiallergic drug. RESULTS: It has been demonstrated that cetirizine is able to reduce ICAM-1 expression on nasal epithelial cells and conjunctival nonspecific hyperreactivity in asthmatic asymptomatic children with MPI. CONCLUSIONS: The therapeutical strategy of mite allergy should be targeted to treat minimal persistent inflammation.