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Updated: Mar 2, 2026

Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells
Published on: March 23, 2022
The expression of NKG2D on porcine IEL and its possible relation to the adaptive intestinal immune system
Sara Altmeyer1, Jürgen Zentek1, Wilfried Vahjen1
1Institute of Animal Nutrition, Department of Veterinary Medicine, Freie Universität Berlin, Königin-Luise-Strasse 49, D-14195 Berlin, Germany.
Abstract:
The gastrointestinal tract contains a multitude of components which include intraepithelial lymphocytes (IEL). IELs have been reported to express a variety of surface receptors that enable cross talk among various cell populations. The purpose of the reported investigation was to determine which IEL populations express the natural killer cell receptor NKG2D which is an activating receptor that plays a role in cytolytic responses. In a feeding experiment with piglets, IELs were isolated from jejunal tissue at three different stages post weaning. The time dependent development of different cell populations was evaluated and an elevated number of lymphocytes (CD45+) shortly after weaning was observed compared to later time points. The number of T cells (CD3), including cytotoxic T cells (CD8β/CD16-), appeared to be particularly affected by the weaning period. Correlation analysis revealed an association between the NKG2D expression in jejunal tissue and the frequency of lymphocytes, esp. CD8β+ cytotoxic T cells. Gene expression analysis of NKG2D were performed on several isolated IEL populations and support the hypothesis that cytotoxic T cells (CD8β) in the porcine gut epithelium are capable of communicating with the surrounding enterocytes and inducing immune reactions via NKG2D. Unlike previous observations in porcine blood, the γδ T cells of the gut epithelium also showed expression of the stress factor binding NKG2D receptor. Subsequent analysis of the isolated IELs revealed that T cells appear to only express the receptor after isolation with an anti-CD3 mab, indicating that a previous stimulation of the TCR/CD3 complex may reinforce this signal transduction pathway.

