Eosinophilic esophagitis is characterised for a dense infiltration of the esophagus by eosinophilic leukocytes. The disease's origin is a local reaction to different antigens of which the patient presents previous sensitization, acquired by digestive, inhaled or even epicutaneous exposure. The esophagus contains different cellular types resident in its structure, with capability to participate in the capture, processing and antigens' presentation to T lymphocytes, which could initiate a T helper 2-type immunological response mostly mediated by interleukin-5, with a possible T helper 1-type component. Local production of immunoglobulin E could also participate in the pathophysiology of eosinophilic esophagitis, and for this reason, this disease can be considered a mixed-humoural and cell-mediated immunological disturbance. Studies directed to identificate responsible allergens must consider test for determine immunoglobulin E-mediated reactions as well as cell-mediated hyper-responsiveness responses. Main symptom of eosinophilic esophagitis are dysphagia and esophageal food impactations, which are conditioned by endoscopic alterations and motor disturbances objectively demonstrated by manometric recorders. Eosinophil and mast cell's activation and degranulation against responsible antigens cause damage over esophageal epithelium and dynamic disturbances over neuromuscular components in esophageal wall. Therapies proposed for eosinophilic esophagitis include control of antigen exposition, endoscopic dilation of stenosis and drugs with antieosinophilic effect; in this group topical steroids can be outlined for the capacity of them to restore the histology and the esophageal motility in parallel to vanishment of inflammation.