Celiac disease (CeD) is a widespread, gluten-induced, autoimmune disorder that lacks any medicinal therapy. Towards the goal of developing non-dietary treatments for CeD, research has focused on elucidating its molecular and cellular etiology. A model of pathogenesis has emerged centered on interactions between three molecular families: specific class II MHC proteins on antigen-presenting cells (APCs), deamidated gluten-derived peptides, and T cell receptors (TCRs) on inflammatory CD4⁺ T cells. Growing evidence suggests that this pathogenic axis can be pharmacologically targeted to protect patients from some of the adverse effects of dietary gluten. Further studies have revealed the existence of additional host and environmental contributors to disease initiation and tissue damage. This review summarizes our current understanding of CeD pathogenesis and how it is being harnessed for therapeutic design and development.

乳糜泻 (CeD) 是一种广泛存在的、由麸质引起的自身免疫性疾病，缺乏任何药物治疗。为了开发针对 CeD 的非饮食疗法，研究重点是阐明其分子和细胞病因。一个以三个分子家族之间相互作用为中心的发病机制模型已经出现：抗原呈递细胞 (APC) 上的特定 II 类 MHC 蛋白、脱酰胺麸质衍生肽和炎症 CD4 ⁺ T 细胞上的 T 细胞受体 (TCR)。越来越多的证据表明，这种致病轴可以在药理学上有针对性地保护患者免受膳食麸质的一些不利影响。进一步的研究表明，存在导致疾病发生和组织损伤的其他宿主和环境因素。这篇综述总结了我们目前对 CeD 发病机制的理解以及如何利用它进行治疗设计和开发。