Department of Medical and Biological Science, University of Udine, 33100 Udine, Italy.
Second Unit of Internal Medicine, University Hospital of Udine, 33100 Udine, Italy.
Int J Mol Sci. 2019 Jul 11;20(14):3400. doi: 10.3390/ijms20143400.
Over the last decades, there has been an impressive progress in our understanding of coeliac disease pathogenesis and it has become clear that the disorder is the final result of complex interactions of environmental, genetic, and immunological factors. Coeliac disease is now considered a prototype of T-cell-mediated disease characterized by loss of tolerance to dietary gluten and the targeted killing of enterocytes by T-cell receptor αβ intraepithelial lymphocytes. Accumulating evidence, however, indicates that the induction of a gluten-specific T helper-1 response must be preceded by the activation of the innate immune system. Mast cells are key players of the innate immune response and contribute to the pathogenesis of a multitude of diseases. Here, we review the results of studies aimed at investigating the role of mast cells in the pathogenesis of coeliac disease, showing that these cells increase in number during the progression of the disease and contribute to define a pro-inflammatory microenvironment.
在过去的几十年中，我们对乳糜泻发病机制的理解取得了令人瞩目的进展，很明显，这种疾病是环境、遗传和免疫因素复杂相互作用的最终结果。乳糜泻现在被认为是 T 细胞介导疾病的典型代表，其特征是对膳食 gluten 的耐受性丧失，以及 T 细胞受体 αβ 上皮内淋巴细胞对肠细胞的靶向杀伤。然而，越来越多的证据表明，对 gluten 的特异性 T 辅助-1 反应的诱导必须先于固有免疫系统的激活。肥大细胞是固有免疫反应的关键参与者，并有助于多种疾病的发病机制。在这里，我们回顾了旨在研究肥大细胞在乳糜泻发病机制中的作用的研究结果，表明这些细胞在疾病进展过程中数量增加，并有助于定义促炎微环境。
