ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Brain glycolipids suppress T helper cells and inhibit autoimmune demyelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota.Cell metabolism · 2018Trial
- Altered Lipid Metabolism in CNS Demyelination and Remyelination Are Key Elements Driving Progressive MS.International journal of molecular sciences · 2025Review
- Possible Roles of Extracellular Vesicles in the Pathogenesis and Interventions of Immune-Mediated Central Demyelinating Diseases.Experimental neurobiology · 2024Review
- The immune system in neurological diseases: What innate-like T cells have to say.The Journal of allergy and clinical immunology · 2024Review
- Immunological role of sulfatide in the pathogenesis of multiple sclerosis.Neural regeneration research · 2023Article
- Anti-Glycolipid Antibody Examination in Five EAE Models and Theiler's Virus Model of Multiple Sclerosis: Detection of Anti-GM1, GM3, GM4, and Sulfatide Antibodies in Relapsing-Remitting EAE.International journal of molecular sciences · 2023Article
- T cells from MS Patients with High Disease Severity Are Insensitive to an Immune-Suppressive Effect of Sulfatide.Molecular neurobiology · 2022Article
- The etiology and pathogenesis of type 1 diabetes - A personal, non-systematic review of possible causes, and interventions.Frontiers in endocrinology · 2022Review
- 3'-Sulfo-TF Antigen Determined by GAL3ST2/ST3GAL1 Is Essential for Antitumor Activity of Fungal Galectin AAL/AAGL.ACS omega · 2021Article
- New Insights into Multiple Sclerosis Mechanisms: Lipids on the Track to Control Inflammation and Neurodegeneration.International journal of molecular sciences · 2021Review
- Strength Exercise Confers Protection in Central Nervous System Autoimmunity by Altering the Gut Microbiota.Frontiers in immunology · 2021Article
- The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis.Cellular and molecular life sciences : CMLS · 2020Review
- Don't sugarcoat it: How glycocalyx composition influences cancer progression.The Journal of cell biology · 2020Review
- Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis.International journal of molecular sciences · 2018Review
- The Role of 3-O-Sulfogalactosylceramide, Sulfatide, in the Lateral Organization of Myelin Membrane.Neurochemical research · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CNS is considered an immune privileged site because its repertoire of highly immunogenic molecules remains unseen by the immune system under normal conditions. However, the mechanism underlying the inhibition of immune reactions within the CNS environment is not known, particularly in regions containing myelin, which contains several potent proteins and lipids that are invariably recognized as foreign by immune system cells. Sulfatides constitute a major component of myelin glycolipids and are known to be capable of raising an immune response. In this study, the effect of sulfatides on mouse T cell function and differentiation was analyzed in vitro and in vivo. We found profound inhibition of sulfatide-dependent T cell proliferation which was particularly pronounced in naive T helper (Th) cells. The inhibitory effect of sulfatides on T cell function was CD1d-independent and was not related to apoptosis or necrosis but did involve the induction of anergy as confirmed by the upregulation of early growth response 2 transcription factor. A glycolipid 3-sulfate group was essential for the T cell suppression, and the T cell inhibition was galectin-4-dependent. Sulfatide stimulation in vitro led to prominent suppression of Th17 differentiation, and this was related to a decrease in susceptibility to disease in a mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis. Thus, we have defined a novel mechanism of negative regulation of T cell function by endogenous brain-derived glycolipids, a family of molecules traditionally deemphasized in favor of myelin proteins in studies of CNS autoimmunity.
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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.