Department of Gastroenterology, Hospital General de Tomelloso, Tomelloso, Ciudad Real, Spain.
Expert Rev Gastroenterol Hepatol. 2014 Aug;8(6):669-85. doi: 10.1586/17474124.2014.909727. Epub 2014 Apr 18.
Eosinophilic esophagitis (EoE) is a pathophysiologically complex disorder driven by distinct, multiple mechanisms involving a large number of cells, molecules, and genes. Associated with food allergy from its initial descriptions, a key role for the Th2-type cytokines IL-5 and IL-13 in recruiting and activating eosinophils has been described. Epithelial cells have been recognized as major effectors in initiating EoE, both through their recruitment of iNKT cells towards the esophageal epithelium, which constitutes a major cytokine source, and through the release of eotaxin-3 and other chemoattractants. Epithelial and mesenchymal-released TSLP is a key regulator for which a connecting role between the adaptive and innate mucosal-associated immune response has been suggested. Finally, activated eosinophil- and mast cell-derived TGF β1 secretion is crucial in EoE-associated tissue remodeling.
嗜酸性食管炎（EoE）是一种病理生理复杂的疾病，由涉及大量细胞、分子和基因的不同、多种机制驱动。从最初的描述中可以看出，与食物过敏有关，Th2 型细胞因子 IL-5 和 IL-13 在招募和激活嗜酸性粒细胞方面发挥了关键作用。上皮细胞已被认为是引发 EoE 的主要效应细胞，这既通过其招募 iNKT 细胞朝向食管上皮，这构成了主要的细胞因子来源，也通过释放 eotaxin-3 和其他趋化因子。上皮细胞和间充质细胞释放 TSLP 是一个关键的调节剂，提示适应性和固有黏膜相关免疫反应之间存在连接作用。最后，激活的嗜酸性粒细胞和肥大细胞衍生的 TGFβ1 分泌在 EoE 相关的组织重塑中至关重要。
