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IL-4, IL-13, and IL-5 drive the complex pathophysiology of eosinophilic esophagitis (EoE)1-7

IL-4, IL-13, and IL-5 are key Type 2 cytokines in EoE, secreted by cells of the innate and adaptive immune systems1-6

Th0 cell differentiation to Th2
B cell class switching and IgE production
Fibrosis, tissue remodeling, and increased smooth muscle contraction
Increased barrier disruption
Eosinophil trafficking to tissues
Eosinophil differentiation in the bone marrow
IL-4, IL-13, and IL-5 may contribute to immune system overreaction, as
well as esophageal remodeling, a characteristic of EoE, including
fibrosis and epithelial hyperplasia8,9

ILC2, type 2 innate lymphoid cells; PGD2, prostaglandin D2; TSLP, thymic stromal lymphopoietin.

References: 1. Hill DA, Spergel JM. The immunologic mechanisms of eosinophilic esophagitis. Curr Allergy Asthma Rep. 2016;16(2):9. doi:10.1007/s11882-015-0592-3 2. Gandhi NA, Bennett BL, Graham NMH, Pirozzi G, Stahl N, Yancopoulos GD. Targeting key proximal drivers of type 2 inflammation in disease. Nat Rev Drug Discov. 2016;15(1):35-50. 3. Furuta GT, Katzka DA. Eosinophilic esophagitis. N Engl J Med. 2015;373(17):1640-1648. 4. D’Alessandro A, Esposito D, Pesce M, Cuomo R, De Palma GD, Sarnelli G. Eosinophilic esophagitis: from pathophysiology to treatment. World J Gastrointest Pathophysiol. 2015;6(4):150-158. 5. Davis BP, Rothenberg ME. Mechanisms of disease of eosinophilic esophagitis. Annu Rev Pathol. 2016;11:365-393. 6. Malhotra N, Levine J. Eosinophilic esophagitis: an autoimmune esophageal disorder. Curr Probl Pediatr Adolesc Health Care. 2014;44(11):335-340. 7. Siracusa MC, Kim BS, Spergel JM, Artis D. Basophils and allergic inflammation. J Allergy Clin Immunol. 2013;132(4):789-801. 8. Muir AB, Wang JX, Nakagawa H. Epithelial-stromal crosstalk and fibrosis in eosinophilic esophagitis. J Gastroenterol. 2019;54(1):10-18. 9. Cheng E, Souza RF, Spechler SJ. Tissue remodeling in eosinophilic esophagitis. Am J Physiol Gastrointest Liver Physiol. 2012;303(11):G1175-G1187.