We thank Drs Nonevski, Fiocchi, and Falk for their excellent summary and provocative ideas about the implications of our study. Our working model is that food antigen-driven Th2 cell-derived IL-13 induces esophageal keratinocytes to overproduce eotaxin-3. It is intriguing that IL-4 appears to be less important and that eotaxin-1 and eotaxin-2 are not coproduced in this disease or by IL-13 stimulation of esophageal keratinocytes. We are actively pursuing experiments aimed at elucidating the molecular mechanisms that are responsible for this selective signaling and the beneficial effect of certain therapeutic interventions (eg, diet and corticosteroids). We are hopeful that uncovering the molecular mysteries of this enigmatic disease will provide better therapy for the growing number of individuals suffering from eosinophilic disorders. Eosinophilic esophagitis: New insights into an emerging diseaseGastroenterologyVol. 131Issue 6PreviewBlanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa’ad AH, Putnam PE, Aronow BJ, Rothenberg ME. (Division of Allergy and Immunology Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio). Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest 2006;116:536–547. Full-Text PDF