Abstract
The role of intestinal epithelial cells (IECs) in mucosal tolerance and immunity remains poorly understood. We present a method for inducing MHC class II (MHC-II) in human enteroids, “mini-guts” derived from small intestinal crypt stem cells, and show that the intracellular MHC-II peptide-pathway is intact and functional in IECs. Our approach enables human enteroids to be used for novel in vitro studies into IEC MHC-II regulation and function during health and disease.
Highlights
Intestinal epithelial cells (IECs) are well-positioned to interact with both the gut microbial and dietary milieu as well as the underlying mucosal immune system
We showed that treatment with interferon gamma (IFNg) induced Major Histocompatibility Complex II (MHC-II) protein
We present a method for inducing MHC-II in human intestinal enteroids in a physiologically relevant manner
Summary
Intestinal epithelial cells (IECs) are well-positioned to interact with both the gut microbial and dietary milieu as well as the underlying mucosal immune system. Numerous prior reports show that IECs constitutively express Major Histocompatibility Complex II (MHC-II), a key molecule in the stimulation of CD4+ T cell responses [1,2,3]. This raises the possibilities that IECs contribute to tolerance and immunity through MHC-II-mediated antigen presentation and that IEC MHC-II is involved in intestinal disorders, such as inflammatory bowel and celiac disease. Standard colonic cell lines—including T84, Caco-2, and HT29—are problematic because MHC-II is expressed in the small intestine, but not the colonic epithelium under non-inflammatory conditions [5]. These adenocarcinoma-derived cell lines possess epigenetic modifications known to alter MHC-II expression [6]
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