对于乳糜泻的发病机制，除了免疫细胞成分外，还包括十二指肠上皮中的病理事件。在乳糜泻患者中，饮食中的麸质暴露会导致上皮细胞分化发生剧变，并引发对炎症细胞因子的细胞反应。乳糜泻的自身抗原转谷氨酰胺酶2 (TG2) 酶据推测也在肠上皮中发挥其致病性麦胶蛋白脱氨基化事件作用。因此，过去利用体外上皮细胞系模型研究这些致病机制，但一直受到其简化性质以及缺乏正确细胞类型组成和肠环境的影响。此外，这些细胞模型也存在许多与肿瘤抑制基因相关的癌变突变，使其不适合研究细胞分化。肠器官样团提供了一种接近天然上皮细胞模型，用于研究与乳糜泻相关的致病因子和机制。在这里，我们描述了初始化和维持乳糜泻患者衍生的器官样团培养的协议，以及如何以不同的方式培养它们，使其能够在不同类型的实验中得到应用。版权所有 © 2023 Elsevier Inc. 保留所有权利。

Celiac disease pathogenesis, in addition to immune cell component, encompasses pathogenic events also in the duodenal epithelium. In celiac disease patients, exposure to dietary gluten induces drastic changes in epithelial differentiation and elicit cellular response to inflammatory cytokines. The autoantigen in celiac disease, transglutaminase 2 (TG2) enzyme, has been also suggested to play its pathogenic gliadin deamidation event in the intestinal epithelium. Therefore in vitro epithelial cell-line models have been exploited in the past to study these pathogenic mechanisms, but they are hampered by their simplistic nature lacking proper cell-type composition and intestinal environ. Moreover, these cell models harbor many cancer-related mutations in tumor suppressor genes making them unsuitable for studying cell differentiation. Intestinal organoids provide a near-native epithelial cell model to study pathogenic agents and mechanisms related to celiac disease. Here we describe protocols to initiate and maintain celiac patient-derived organoid cultures and how to grow them in alternative ways allowing their exploitation in different kind of experiments.Copyright © 2023 Elsevier Inc. All rights reserved.