“…The early phase reaction leads to a late phase after 6–12 h that is sustained by T‐cell‐dependent processes through the production of cytokines and chemokines that mediate the recruitment and conjunctival infiltration of eosinophils and other immune cells (Choi and Bielory, ). This latter event requires the interaction between leukocyte surface‐adhesion receptors, such as integrins and selectins, and adhesion molecules expressed on the conjunctival endothelium, such as intercellular adhesion molecule‐1 (ICAM‐1) (Oh et al, ) and vascular cell adhesion molecule‐1 (VCAM‐1) (Baiula et al, ). Increased levels of cell adhesion molecules on the microvasculature and factors that regulate these molecules may perpetuate inflammation in allergic conjunctivitis (Okada et al, ).…”