Celiac Disease (CeD) is an immune-mediated complex disease that is triggered by the ingestion of gluten and develops in genetically susceptible individuals. It has been known for a long time that the Human Leucocyte Antigen (HLA) molecules DQ2 and DQ8 are necessary, although not sufficient, for the disease development, and therefore other susceptibility genes and (epi)genetic events must participate in CeD pathogenesis. The advances in Genomics during the last 15 years have made CeD one of the immune-related disorders with the best-characterized genetic component. In the present work, we will first review the main Genome-Wide Association Studies (GWAS) carried out in the disorder, and emphasize post-GWAS discoveries, including diverse integrative strategies, SNP prioritization approaches, and insights into the Microbiome through the host Genomics. Second, we will explore CeD-related Epigenetics and Epigenomics, mostly focusing on the emerging knowledge of the celiac methylome, and the vast but yet under-explored non-coding RNA (ncRNA) landscape. We conclude that much has been done in the field although there are still completely unvisited areas in the post-Genomics of CeD. Chromatin conformation and accessibility, and Epitranscriptomics are promising domains that need to be unveiled to complete the big picture of the celiac Genome.

乳糜泻 (CeD) 是一种免疫介导的复杂疾病，由摄入麸质引发并在遗传易感个体中发展。人类白细胞抗原（HLA）分子 DQ2 和 DQ8 是疾病发展所必需的，尽管还不够，因此其他易感基因和（表观）遗传事件必须参与 CeD 发病机制。过去 15 年中基因组学的进步使 CeD 成为具有最佳遗传成分的免疫相关疾病之一。在目前的工作中，我们将首先回顾在该疾病中开展的主要全基因组关联研究 (GWAS)，并强调 GWAS 后的发现，包括各种综合策略、SNP 优先级方法以及通过宿主基因组学对微生物组的洞察. 其次，我们将探索与 CeD 相关的表观遗传学和表观基因组学，主要关注腹腔甲基化组的新兴知识，以及广阔但尚未探索的非编码 RNA (ncRNA) 领域。我们得出的结论是，尽管在 CeD 的后基因组学中仍有一些完全未被访问的领域，但该领域已经做了很多工作。染色质构象和可及性以及表观转录组学是有希望的领域，需要揭开它们的面纱，以完成乳糜泻基因组的全貌。