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. 2018 Jun 18;9:1324. doi: 10.3389/fimmu.2018.01324

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Copyright © 2018 Hosomi, Grootjans, Huang, Kaser and Blumberg.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Endoplasmic reticulum (ER) stress-inducing murine UL16-binding protein like transcript 1 (MULT1) in mouse. MULT1 [encoded by UL16 binding protein 1 (Ulbp1)], but not other natural-killer group 2 member D (NKG2D)-ligands, mRNA, and surface expression are upregulated on ER-stressed mouse small intestinal epithelial cells. This occurs through activating factor 4 (ATF4) and/or C/EBP homologous protein (CHOP) presumably downstream of the protein kinase RNA-like ER kinase pathway. CHOP as a transcription factor binds directly to the promoter area of Ulbp1, which upon expression subsequently activates NKG2D-expressing intraepithelial group 1 innate lymphoid cells (ILCs) [natural killer (NK) cells and ILC1] that accumulate within the intestinal epithelium and promote small intestinal inflammation.