ArticleImmunogenetics2010
Inhibition of type 1 diabetes by upregulation of the circadian rhythm-related aryl hydrocarbon receptor nuclear translocator-like 2.
Article in Immunogenetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.Annals of medicine · 2025Review
- Single-cell resolution of intestinal regeneration in pythons without crypts illuminates conserved vertebrate regenerative mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Deletion of the Clock GeneThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Therapeutic potential of aryl hydrocarbon receptor in autoimmunity.Inflammopharmacology · 2020Review
- DEC2 Blocks the Effect of the ARNTL2/NPAS2 Dimer on the Expression of PER3 and DBP.Journal of circadian rhythms · 2017Article
- Air Travel, Circadian Rhythms/Hormones, and Autoimmunity.Clinical reviews in allergy & immunology · 2017Review
- The circadian gene Arntl2 on distal mouse chromosome 6 controls thymocyte apoptosis.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
- Candidate SNP Markers of Chronopathologies Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters.BioMed research international · 2016Article
- Global effect of interleukin-10 on the transcriptional profile induced by Neisseria meningitidis in human monocytes.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic locus Idd6 is involved in type 1 diabetes development in the non-obese diabetic (NOD) mouse through its effect on the immune system and in particular, on T cell activities. Analysis of congenic strains for Idd6 has established the Aryl hydrocarbon receptor nuclear translocator-like 2 (Arntl2) as a likely candidate gene. In this study we investigate the role of Arntl2 in the autoimmune disease and T cell activation. An Arntl2 expressing plasmid was transfected into CD4(+) T cells by nucleofection. Expression levels of cytokines and CD4(+) T cell activation markers, cell death, apoptosis, and cell proliferation rates were characterized in ex vivo experiments whilst in vivo the transfected cells were transferred into NOD.SCID mice to monitor diabetes development. The results demonstrate that Arntl2 overexpression leads to inhibition of CD4(+) T cell proliferation and decreases in their diabetogenic activity without influence on the expression levels of cytokines, CD4(+) T cell activation markers, cell death, and apoptosis. Our findings suggest that Arntl2 at the Idd6 locus may act via the inhibition of CD4(+) T cell proliferation and the reduction in the diabetogenic activity of CD4(+) T cells to protect against autoimmune type 1 diabetes in the NOD mice.
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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.