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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: J Allergy Clin Immunol. 2018 May 31;142(1):24–31.e2. doi: 10.1016/j.jaci.2018.05.018

Figure.

Figure

Therapeutic targets for current and future biologics in eosinophilic esophagitis. Basophils and antigen-presenting cells mediate dietary antigen presentation to naïve T-cells (Th0), which through TSLP and IL-4 drives T-helper cell Type 2 (Th2) cell expansion. Th2 are recruited to the esophagus via integrins and prostaglandins and drive B-cell production of immunoglobulins, along with mast cell hyperplasia. Th2 cells secrete IL-5 which further enhances eosinophil recruitment via release of eotaxins and eosinophil survival. Th2 cells secrete IL-13, which dysregulates the epithelium to recruit Th2 inflammatory cells and promotes remodeling. Eosinophils and mast cells are effector cells that are activated to secrete proteases, cytokines and histamine which drive mucosal inflammatory changes and symptoms. TGF-β1 has a key role in fibrosis. Specific targets discussed include: 1) IL-5R, 2) Eotaxins, 3) IL4R/IL13, 4) CRTH2, 5) TSLP, 6) Siglec-8, 7) IgE, 8) TGF-β1, 9) Integrin α4β1/7