ArticlePloS one2012
NK cells are not required for spontaneous autoimmune diabetes in NOD mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- IL-21 mediates crosstalk between T cells and NK cells during the remission of type 1 diabetes.Nature metabolism · 2026Article
- Lower percentages of natural killer cells in children with type 1 diabetes and their siblings.Pediatric endocrinology, diabetes, and metabolism · 2023Article
- Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021Review
- Innate inflammation drives NK cell activation to impair Treg activity.Journal of autoimmunity · 2020Article
- The Four-Way Stop Sign: Viruses, 12-Lipoxygenase, Islets, and Natural Killer Cells in Type 1 Diabetes Progression.Frontiers in endocrinology · 2017Article
- The Expanding Role of Natural Killer Cells in Type 1 Diabetes and Immunotherapy.Current diabetes reports · 2016Review
- Flow cytometric gating for spleen monocyte and DC subsets: differences in autoimmune NOD mice and with acute inflammation.Journal of immunological methods · 2016Article
- Depletion of IL-2 receptor β-positive cells protects from diabetes in non-obese diabetic mice.Immunology and cell biology · 2016Article
- Tissue-Resident NK Cells Mediate Ischemic Kidney Injury and Are Not Depleted by Anti-Asialo-GM1 Antibody.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Article
- Type 1 diabetes: translating mechanistic observations into effective clinical outcomes.Nature reviews. Immunology · 2013Review
- Type 1 diabetes therapy beyond T cell targeting: monocytes, B cells, and innate lymphocytes.The review of diabetic studies : RDS · 2012Review
- Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.The review of diabetic studies : RDS · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
NK cells have been shown to either promote or protect from autoimmune diseases. Several studies have examined the role of receptors preferentially expressed by NK cells in the spontaneous disease of NOD mice or the direct role of NK cells in acute induced disease models of diabetes. Yet, the role of NK cells in spontaneous diabetes has not been directly addressed. Here, we used the NOD.NK1.1 congenic mouse model to examine the role of NK cells in spontaneous diabetes. Significant numbers of NK cells were only seen in the pancreas of mice with disease. Pancreatic NK cells displayed an activated surface phenotype and proliferated more than NK cells from other tissues in the diseased mice. Nonetheless, depletion of NK cells had no effect on dendritic cell maturation or T cell proliferation. In spontaneous disease, the deletion of NK cells had no significant impact on disease onset. NK cells were also not required to promote disease induced by adoptively transferred pathogenic CD4(+) T cells. Thus, NK cells are not required for spontaneous autoimmune diabetes in NOD mice.
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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.