B cells, IgE and mechanisms of type I hypersensitivity in eosinophilic oesophagitis

The pathogenesis of eosinophilic oesophagitis (EO) is unknown. EO has recently been defined as significantly elevated intraepithelial eosinophils (⩾15 per high-power field) throughout the oesophageal mucosa, coupled with clinical and endoscopic signs of oesophagitis that cannot be attributed to gastro-oesophageal reflux disease (GORD) or other causes.1 2 This inflammatory condition is more likely to occur in atopic individuals and is limited to the oesophagus where Th2 cytokines and mast cells are also abnormally elevated.1 Removal of specific protein or all proteins from the diet may resolve the inflammatory response in some patients.3 Animal models point to antigen exposure in lung or nasal mucosa leading to local inflammation and oesophagitis.4 EO may indeed be the manifestation of an oesophageal hypersensitivity response to food or environmental antigens, but since a systemic response is not present, local mucosal immune events may be important in this disease. Patients with EO have increased numbers of cells required for local immunoglobulin E (IgE) antibody production. Lucendo et al used sensitive immunohistochemical evaluation to quantify B cells (CD20+);5 however, very few intraepithelial B cells were detected in oesophagitis (EO and GORD), and the numbers did not reach statistical significance. Mucosal mast cells are also increased in the oesophagus in EO, and these cells stain positively for IgE.5 6 7 …