ArticleJournal of immunology (Baltimore, Md. : 1950)2008
NKG2D-RAE-1 receptor-ligand variation does not account for the NK cell defect in nonobese diabetic mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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
10 citing papers in PubMed, 13 citations in OpenAlex.
- Reevaluation of NOD/SCID Mice as NK Cell-Deficient Models.BioMed research international · 2021Article
- The Four-Way Stop Sign: Viruses, 12-Lipoxygenase, Islets, and Natural Killer Cells in Type 1 Diabetes Progression.Frontiers in endocrinology · 2017Article
- Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.PLoS neglected tropical diseases · 2014Article
- A gluten-free diet lowers NKG2D and ligand expression in BALB/c and non-obese diabetic (NOD) mice.Clinical and experimental immunology · 2014Article
- Mechanisms of NK cell-macrophage Bacillus anthracis crosstalk: a balance between stimulation by spores and differential disruption by toxins.PLoS pathogens · 2012Article
- Natural killer cells recognize friend retrovirus-infected erythroid progenitor cells through NKG2D-RAE-1 interactions In Vivo.Journal of virology · 2011Article
- Innate immunity and the pathogenesis of type 1 diabetes.Seminars in immunopathology · 2011Review
- Article
- A defective Il15 allele underlies the deficiency in natural killer cell activity in nonobese diabetic mice.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The activating receptor NKp46 is essential for the development of type 1 diabetes.Nature immunology · 2010Article
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 1 institution in 2 countries.
Funding
Abstract
NK cells from NOD mice induced with poly(I:C) in vivo exhibit low cytotoxicity against a range of target cells, but the genetic mechanisms controlling this defect are yet to be elucidated. Defects in the expression of NKG2D and its ligands, the RAE-1 molecules, have been hypothesized to contribute to the reduced NK function present in NOD mice. In this study, we show that segregation of the NK-mediated killing phenotype did not correlate with the NOD Raet1 haplotype and that the large alterations in NKG2D expression previously reported on NK cells expanded in vitro were not observed in primary, poly(I:C)-elicited NK cells in vivo. Additional studies indicate a complex genetic control of defective NOD NK cells including genes linked to the MHC and possibly those that are associated with an altered cytokine response to the TLR3-agonist poly(I:C).
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Identifiers
What OpenQuestion holds
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.