Coeliac disease (CeD) is an autoimmune disorder in which gluten digestion in patients expressing MHC class II human leukocyte antigen molecules (HLA)-DQ2 or HLA-DQ8 promotes immune-mediated duodenal mucosa damage. As with other autoimmune conditions, CeD research is hampered by the lack of a model system that maintains structural integrity of the affected epithelium and the associated immune cell milieu. In a recent study, Santos et al.  describe their development of a human air-liquid interface (ALI) CeD organoid model derived from endoscopic biopsies that preserves the relevant epithelial, mesenchymal, and immune cell populations (1). Using this model, they reveal how interleukin-7 (IL-7) drives gluten-induced epithelial damage by stimulating the expression of NKG2C/D in CD8⁺ T cells. Their work validates the use of organoids in autoimmunity research to accelerate mechanistic understanding and therapeutics screening for CeD and other related disorders.

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Reference:

1. Nature. 2024 Aug;632(8024):401-410. doi: 10.1038/s41586-024-07716-2.