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. 2022 Jul 25;71(11):2337–2349. doi: 10.1136/gutjnl-2021-326257

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Activation of cytotoxic intraepithelial lymphocytes and induction of tissue damage in active coeliac disease (CD). Cooperation between the cytokines released by activated gluten-specific CD4⁺ T cells and interleukin (IL)-15 produced by epithelial and myeloid cells drive the activation of cytotoxic CD8⁺ T intraepithelial lymphocytes (IEL) and license epithelial cell killing. Cytotoxic CD8⁺ T IEL synthesise interferon gamma (IFNγ) and cytotoxic molecules such as granzyme B and perforin, upregulate the activating natural killer receptor NKG2D and CD94/NKG2C, thereby facilitating the interactions of cytotoxic CD8⁺ T IEL with enterocytes which, in active CD, display MICA (MHC class I polypeptide-related sequence A), the ligand of NKG2D (induced by tissue stress) and HLA-E, the ligand of NKG2C (induced by IFNγ). DC, dendritic cell; TCR, T cell receptor; TGF-β, transforming growth factor beta; Treg, regulatory T cell. Created with Biorender.com.