In recent years, a complex molecular network involving cytokines kinins and adhesion molecules has been demonstrated to operate in allergic inflammation. In particular, the adhesion machinery plays a crucial role for the recruitment and locomotion of the inflammatory cells and the Intercellular Adhesion Molecule 1 (ICAM-1) is a hallmark of the allergic inflammatory process. The role and possible modulation of ICAM-1 can be investigated using both eye and nose experimental models. Conjunctival and nasal epithelium are easy to study either under natural allergen exposure or after specific/aspecific provocation tests; furthermore the nasal/conjunctival challenge is well tolerated by the patients. These experimental models have allowed us to investigate in vivo the antiallergic properties of several compounds. Many of the new antihistamines, but also deflazacort and local nasal immunotherapy, were demonstrated capable of reducing both inflammatory infiltration and ICAM-1 expression on epithelia. Because of the central role of adhesion molecules in allergic inflammation, their pharmacological modulation can be regarded as a promising therapeutic approach.