De Re Valli, Magris Raffaella, Cannizzaro Renato
Immunopatologia e Biomarcatori Oncologici/Bio-Proteomics Facility, CRO Aviano National Cancer Institute, Aviano, Italy.
Oncological Gastroenterology, CRO Aviano National Cancer Institute, Aviano, Italy.
Front Med (Lausanne). 2017 Aug 31;4:137. doi: 10.3389/fmed.2017.00137. eCollection 2017.
Celiac disease (CD) is an autoimmune and multisystem gluten-related disorder that causes symptoms involving the gastrointestinal tract and other organs. Pathogenesis of CD is only partially known. It had been established that ingestion of gluten proteins present in wheat and other cereals are necessary for the disease and develops in individuals genetically predisposed carrying the DQ2 or DQ8 human leukocyte antigen haplotypes. In this review, we had pay specific attention on the last discoveries regarding the three cellular components mainly involved in the development and maintenance of CD: T-cells, B-cells, and microbioma. All of them had been showed critical for the interaction between inflammatory immune response and gluten peptides. Although the mechanisms of interaction among overall these components are not yet fully understood, recent proteomics and molecular studies had shed some lights in the pathogenic role of tissue transglutaminase 2 in CD and in the alteration of the intestinal barrier function induced by host microbiota.
乳糜泻（CD）是一种自身免疫性多系统麸质相关疾病，会引发涉及胃肠道及其他器官的症状。CD的发病机制仅部分为人所知。已经确定，摄入小麦和其他谷物中的麸质蛋白是该疾病发病的必要条件，且在携带DQ2或DQ8人类白细胞抗原单倍型的遗传易感性个体中发病。在本综述中，我们特别关注了关于主要参与CD发生和维持的三种细胞成分的最新发现：T细胞、B细胞和微生物群。所有这些成分都已被证明在炎症免疫反应与麸质肽之间的相互作用中至关重要。尽管这些成分之间的总体相互作用机制尚未完全了解，但最近的蛋白质组学和分子研究已对组织转谷氨酰胺酶2在CD中的致病作用以及宿主微生物群诱导的肠道屏障功能改变有所阐明。
