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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: J Allergy Clin Immunol. 2020 Mar 19;145(6):1629–1640.e4. doi: 10.1016/j.jaci.2020.01.051

FIG 6:

FIG 6:

Summary of study results and proposed disease mechanism. (A) Groups I-V as defined in this study were not statistically different on the basis of eosinophil count but exhibited increased disease severity as assessed by cumulative EDP scoring. Expression of cytokines and chemokines varied among the 5 groups, which also differed in terms of membership in EoE endotypes 1-3. (B) Model depicting patient progression from Th2-low phenotype (congruent with EoEe1) to a Th2-high phenotype (congruent with EoEe2) following allergic or inflammatory insult. Upon steroid treatment, food elimination, or biologic therapy the Th2-gene expression decreases and patients either resolve inflammation by reverting to a Th2-low phenotype or develop a fibrostenotic (EoEe3) signature.