ArticleDiabetes2011
Ganglioside GM1 deficiency in effector T cells from NOD mice induces resistance to regulatory T-cell suppression.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- The sweet and the bitter sides of galectin-1 in immunity: its role in immune cell functions, apoptosis, and immunotherapies for cancer with a focus on T cells.Seminars in immunopathology · 2025Review
- Galectin-1 correlates with inflammatory markers and T regulatory cells in children with type 1 diabetes and/or celiac disease.Clinical and experimental immunology · 2024Article
- Region-specific mouse brain ganglioside distribution revealed by an improved isobaric aminoxyTMT labeling strategy with automated data processing.Analytical and bioanalytical chemistry · 2023Article
- Age-Related Decline in Gangliosides GM1 and GD1a in Non-CNS Tissues of Normal Mice: Implications for Peripheral Symptoms of Parkinson's Disease.Biomedicines · 2023Article
- Subnormal GM1 in PBMCs: Promise for Early Diagnosis of Parkinson's Disease?International journal of molecular sciences · 2021Article
- Review
- LXR directly regulates glycosphingolipid synthesis and affects human CD4+ T cell function.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation: Review of Pathways and Implications for Clinical Practice.Clinical reviews in allergy & immunology · 2021Review
- How galectins have become multifunctional proteins.Histology and histopathology · 2020Review
- Gangliosides Destabilize Lipid Phase Separation in Multicomponent Membranes.Biophysical journal · 2019Article
- Dynamic Immune Phenotypes of B and T Helper Cells Mark Distinct Stages of T1D Progression.Diabetes · 2019Article
- T Regulatory Cells From Non-obese Diabetic Mice Show Low Responsiveness to IL-2 Stimulation and Exhibit Differential Expression of Anergy-Related and Ubiquitination Factors.Frontiers in immunology · 2019Article
- Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis.Infection and immunity · 2018Article
- Transient Receptor Potential Canonical Channels 4 and 5 MediateOxidative medicine and cellular longevity · 2018Article
- Galectins: their network and roles in immunity/tumor growth control.Histochemistry and cell biology · 2017Review
- Lipid glycosylation: a primer for histochemists and cell biologists.Histochemistry and cell biology · 2017Review
- Biochemical and Electrophysiological Modification of Amyloid Transthyretin on Cardiomyocytes.Biophysical journal · 2016Article
- Transient Receptor Potential (TRP) channels in T cells.Seminars in immunopathology · 2016Review
- Sweet complementarity: the functional pairing of glycans with lectins.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo detect GM1 deficiency and determine its role in effector T cells (Teffs) from NOD mice in establishing resistance to regulatory T-cell (Treg) suppression. RESEARCH DESIGN AND
methodsCD4(+) and CD8(+) Teffs were isolated from spleens of prediabetic NOD mice for comparison with similar cells from Balb/c, C57BL/6, and NOR mice. GM1 was quantified with thin-layer chromatography for total cellular GM1 and flow cytometry for cell-surface GM1. Suppression of Teff proliferation was determined by application of GM1 cross-linking agents or coculturing with Tregs. Calcium influx in Teffs was quantified using fura-2.
resultsResting and activated CD4(+) and CD8(+) Teffs of NOD mice contained significantly less GM1 than Teffs from the other three mouse strains tested. After activation, NOD Teffs resisted suppression by Tregs or GM1 cross-linking agents in contrast to robust suppression of Balb/c Teffs; this was reversed by preincubation of NOD Teffs with GM1. NOD Teffs also showed attenuated Ca(2+) influx via transient receptor potential channel 5 (TRPC5) channels induced by GM1 cross-linking, and this, too, was reversed by elevation of Teff GM1.
conclusionsGM1 deficiency occurs in NOD Teffs and contributes importantly to failed suppression, which is rectified by increasing Teff GM1. Such elevation also reverses subthreshold Ca(2+) influx via TRPC5 channels, an essential aspect of suppression. Our results also support a critical role for galectin-1 as a GM1 cross-linking counter-receptor that fittingly is upregulated and released by Tregs during activation. These findings suggest a novel mechanism by which pathogenic Teffs evade regulatory suppression, thereby leading to autoimmune β-cell destruction and type 1 diabetes.
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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.