ArticleImmunity2012
RAE1ε ligand expressed on pancreatic islets recruits NKG2D receptor-expressing cytotoxic T cells independent of T cell receptor recognition.
Article in Immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- A single-cell census of pulmonary endarterectomies tissue across different anatomical regions in chronic thromboembolic pulmonary hypertension.Clinical and translational medicine · 2026Article
- Pathogenic CD8+ T cells target K71+ Henle's layer by forming cytolytic immune synapses in Alopecia Areata.Research square · 2026Article
- Autoimmune CD8+ T cells in type 1 diabetes: from single-cell RNA sequencing to T-cell receptor redirection.Frontiers in endocrinology · 2024Review
- Observational
- CX3CR1 deficiency-induced TIL tumor restriction as a novel addition for CAR-T design in solid malignancies.iScience · 2023Article
- NKG2D signaling regulates IL-17A-producing γδT cells in mice to promote cancer progression.Discovery immunology · 2022Article
- The Role of the NKG2D in Vitiligo.Frontiers in immunology · 2021Review
- NKG2D Signaling Within the Pancreatic Islets Reduces NOD Diabetes and Increases Protective Central Memory CD8Diabetes · 2020Article
- Regulation of murine NK cell exhaustion through the activation of the DNA damage repair pathway.JCI insight · 2019Article
- Article
- The Paradoxical Role of NKG2D in Cancer Immunity.Frontiers in immunology · 2018Review
- More than Decoration: Roles for Natural Killer Group 2 Member D Ligand Expression by Immune Cells.Frontiers in immunology · 2018Review
- NKG2D: A Master Regulator of Immune Cell Responsiveness.Frontiers in immunology · 2018Review
- NKG2D and Its Ligands: "One for All, All for One".Frontiers in immunology · 2018Review
- The Role of Natural Killer Group 2, Member D in Chronic Inflammation and Autoimmunity.Frontiers in immunology · 2018Review
- A Protective Role for NKG2D-H60a Interaction via Homotypic T Cell Contact in Nonobese Diabetic Autoimmune Diabetes Pathogenesis.ImmunoHorizons · 2017Article
- Anti-NKG2D mAb: A New Treatment for Crohn's Disease?International journal of molecular sciences · 2017Review
- NKG2D ligand expression in Crohn's disease and NKG2D-dependent stimulation of CD8Experimental and molecular pathology · 2017Article
- NK1.1Journal of cellular and molecular medicine · 2017Article
- The immunoreceptor NKG2D promotes tumour growth in a model of hepatocellular carcinoma.Nature communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The mechanisms by which cytotoxic T lymphocytes (CTLs) enter and are retained in nonlymphoid tissue are not well characterized. With a transgenic mouse expressing the NKG2D ligand retinoic acid early transcript 1ε (RAE1ε) in β-islet cells of the pancreas, we found that RAE1 expression was sufficient to induce the recruitment of adoptively transferred CTLs to islets. This was dependent on NKG2D expression by the CTLs and independent of antigen recognition. Surprisingly, the recruitment of CTLs resulted in the subsequent recruitment of a large number of endogenous lymphocytes. Whereas transgenic mice did not develop diabetes, RAE1 expression was sufficient to induce insulitis in older, unmanipulated transgenic mice that was enhanced by viral infection and pancreatic inflammation. These results demonstrate that the expression of an NKG2D ligand in islets is sufficient to recruit CTLs regardless of their antigen specificity and to induce insulitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.