CLDN1 and inflammatory bowel disease: In addition to Wilcz-Villega et al. [35] study showed that a MCs tryptase increased permeability to macromolecules and decreased resistance in a CaCO2 epithelial cell layer system, our results further demonstrated that MCs-derived exosomes reduced ZO-1, OCLN and CLDN1 expression, leading to destroy intestinal epithelial barrier function, which provided a novel pathway of MCs in IBD.