Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

NKG2D ligand expression in Crohn's disease and NKG2D-dependent stimulation of CD8(+) T cell migration

Research output: Contribution to journalJournal articleResearchpeer-review

  1. CDX2 downregulation is associated with poor differentiation and MMR deficiency in colon cancer

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Intra-tumor heterogeneity of microRNA-92a, microRNA-375 and microRNA-424 in colorectal cancer

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Traces of mercury in organs from primates with amalgam fillings

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Progressive alcohol-related liver fibrosis is characterised by imbalanced collagen formation and degradation

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Using MR elastography to assess portal hypertension and response to beta-blockers in patients with cirrhosis

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Hepatic steatosis associated with exposure to elvitegravir and raltegravir

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

Interaction between the activating NKG2D receptor on lymphocytes and its ligands MICA, MICB, and ULBP1-6 modulate T and NK cell activity and may contribute to the pathogenesis of Crohn's disease (CD). NKG2D ligands are generally not expressed on the cell surface of normal, non-stressed cells, but expression of MICA and MICB in CD intestine has been reported. In this exploratory study, we further characterize the expression of NKG2D and its ligands, including the less well-described ULBP4-6, in CD, and test if NKG2D ligand interactions are involved in the migration of activated T cells into the affected mucosal compartments. Intestinal tissue from CD patients and healthy controls were analyzed by flow cytometry, mass cytometry, and immunohistochemistry for expression of NKG2D and ligands, and for cytokine release. Furthermore, NKG2D-dependent chemotaxis of activated CD8(+) T cells across a monolayer of ligand-expressing human intestinal endothelial cells was examined. Activated lymphocytes down-regulated NKG2D expression upon accumulation in inflamed CD intestine. NKG2D expression on CD56(+) T and γδ T cells from inflamed tissue seemed inversely correlated with CRP levels and cytokine release. B cells, monocytes, mucosal epithelium, and vascular endothelium expressed NKG2D ligands in inflamed CD intestine. The expression of NKG2D ligands was correlated with cytokine release, but was highly variable between patients. Stimulation of vascular intestinal endothelial cells in vitro induced expression of NKG2D ligands, including MICA/B and ULBP2/6. Blockade of NKG2D on CD8(+) T cells inhibited the migration over ligand-expressing endothelial cells. Intestinal induction of NKG2D ligands and ligand-induced down-regulation of NKG2D in CD suggest that the NKG2D-ligand interaction may be involved in both the activation and recruitment of NKG2D(+) lymphocytes into the inflamed CD intestine.

Original languageEnglish
JournalExperimental and Molecular Pathology
Volume103
Issue number1
Pages (from-to)56-70
ISSN0014-4800
DOIs
Publication statusPublished - 1 Aug 2017

    Research areas

  • Journal Article

ID: 51518620