ArticleDiabetes2009
Genetic deficiency of Itgb2 or ItgaL prevents autoimmune diabetes through distinctly different mechanisms in NOD/LtJ mice.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Molecular Footprints of the Immune Assault on Pancreatic Beta Cells in Type 1 Diabetes.Frontiers in endocrinology · 2020Pooled it
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- Identification and validation of immune and oxidative stress-related diagnostic markers for diabetic nephropathy by WGCNA and machine learning.Frontiers in immunology · 2023Article
- Identification of Type 2 Diabetes Based on a Ten-Gene Biomarker Prediction Model Constructed Using a Support Vector Machine Algorithm.BioMed research international · 2022Article
- Integrated bioinformatics analysis reveals novel key biomarkers in diabetic nephropathy.SAGE open medicine · 2022Article
- Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis.BMC cardiovascular disorders · 2021Article
- Investigation of the underlying genes and mechanism of familial hypercholesterolemia through bioinformatics analysis.BMC cardiovascular disorders · 2020Article
- Immune cell trafficking to the islets during type 1 diabetes.Clinical and experimental immunology · 2019Review
- System network analysis of genomics and transcriptomics data identified type 1 diabetes-associated pathway and genes.Genes and immunity · 2019Article
- SDF-1-CXCR4 differentially regulates autoimmune diabetogenic T cell adhesion through ROBO1-SLIT2 interactions in mice.Diabetologia · 2013Article
- Absence of β2 integrins impairs regulatory T cells and exacerbates CD4+ T cell-dependent autoimmune carditis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Loss of T cell CD98 H chain specifically ablates T cell clonal expansion and protects from autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Article
- Insulitis in type 1 diabetes: a sticky problem.Diabetes · 2009Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInsulitis is an important pathological feature of autoimmune diabetes; however, mechanisms governing the recruitment of diabetogenic T-cells into pancreatic islets are poorly understood. Here, we determined the importance of leukocyte integrins beta(2)(Itgb2) and alphaL (ItgaL) in developing insulitis and frank diabetes. RESEARCH DESIGN AND
methodsGene-targeted mutations of either Itgb2 or ItgaL were established on the NOD/LtJ mouse strain. Experiments were performed to measure insulitis and diabetes development. Studies were also performed measuring mutant T-cell adhesion to islet microvascular endothelial cells under hydrodynamic flow conditions. T-cell adhesion molecule profiles and adoptive transfer studies were also performed.
resultsGenetic deficiency of either Itgb2 or ItgaL completely prevented the development of hyperglycemia and frank diabetes in NOD mice. Loss of Itgb2 or ItgaL prevented insulitis with Itgb2 deficiency conferring complete protection. In vitro hydrodynamic flow adhesion studies also showed that loss of Itgb2 completely abrogated T-cell adhesion. However, ItgaL deficiency did not alter NOD T-cell adhesion to or transmigration across islet endothelial cells. Adoptive transfer of ItgaL-deficient splenocytes into NOD/Rag-1 mice did not result in development of diabetes, suggesting a role for ItgaL in NOD/LtJ T-cell activation.
conclusionsTogether, these data demonstrate that genetic deficiency of Itgb2 or ItgaL confers protection against autoimmune diabetes through distinctly different mechanisms.
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