CD103 has been shown to be upregulated on intraepithelial lymphocytes and can be induced by TGF-β [40], [41] A higher expression of TGF-β was found in biopsies from healthy children compared to children with Reflux Esophagitis and Eosinophilic Esophagitis, which was in line with the hypothesis that the TGF-β-CD103 axis was disturbed under inflammatory conditions [33]. Here, ITGAE is linked to gastroesophageal reflux disease.