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eosinophilic esophagitis/tyrosine

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The pathogenesis of eosinophilic esophagitis (EoE) is incompletely understood. In certain eosinophilic diseases, activation of tyrosine kinase after fusion of the Fip1-like-1 and platelet-derived growth factor receptor-α genes (F-P fusion gene) mediates eosinophilia via downstream effectors such as

Recent research advances in eosinophilic esophagitis.

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OBJECTIVE Eosinophilic esophagitis (EoE) is a chronic allergic disease triggered by food allergens with an increasing prevalence. This review highlights recent research advances in EoE with a focus on the literature of the past 18 months. RESULTS The incidence of EoE in the black population is
Although interleukin (IL)-13 and neurotrophins are functionally important for the pathogenesis of immune responses, the interaction of these pathways has not been explored. Herein, by interrogating IL-13-induced responses in human epithelial cells we show that neurotrophic tyrosine kinase receptor,

Eosinophilic disorders in children.

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Many pediatric diseases demonstrate blood or tissue eosinophilia. Included among these disorders are common atopic diatheses such as asthma as well as the rarer conditions of hypereosinophilic syndrome and eosinophilic gastrointestinal disorders. Eosinophil trafficking and activation in target

17β-Estradiol protects the esophageal epithelium from IL-13-induced barrier dysfunction and remodeling.

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The incidence of eosinophilic esophagitis (EoE) is greater in male than female subjects, and the underlying molecular basis for this sex bias remains unclear.We sought to delineate the contribution of the sex hormone estrogen to the EoE phenotype and
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