ArticleEuropean journal of immunology2015
Syndecan-1 identifies and controls the frequency of IL-17-producing naïve natural killer T (NKT17) cells in mice.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Heparan Sulfate Proteoglycans in Immunity.Proteoglycan research · 2026Article
- The IL-10-producing NKT10 subset plays a critical role in preventing graft-versus-host-disease.Frontiers in immunology · 2026Article
- Insights into the heterogeneity of iNKT cells: tissue-resident and circulating subsets shaped by local microenvironmental cues.Frontiers in immunology · 2024Review
- Markers and makers of NKT17 cells.Experimental & molecular medicine · 2023Review
- Gene expression profiling in NOD mice reveals that B cells are highly educated by the pancreatic environment during autoimmune diabetes.Diabetologia · 2023Article
- The cytokine receptor DR3 identifies and promotes the activation of thymic NKT17 cells.Cellular and molecular life sciences : CMLS · 2023Article
- The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases.Frontiers in immunology · 2023Review
- CD138 expression is a molecular signature but not a developmental requirement for RORγt+ NKT17 cells.JCI insight · 2021Article
- Calcium signals regulate the functional differentiation of thymic iNKT cells.The EMBO journal · 2021Article
- Syndecan receptors: pericellular regulators in development and inflammatory disease.Open biology · 2021Review
- Lack of Syndecan-1 produces significant alterations in whole-body composition, metabolism and glucose homeostasis in mice.World journal of diabetes · 2020Article
- Recent advances in iNKT cell development.F1000Research · 2020Review
- Article
- Disease Stage-Specific Pathogenicity of CD138 (Syndecan 1)-Expressing T Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2020Article
- Serpinb1a Is Dispensable for the Development and Cytokine Response of Invariant Natural Killer T Cell Subsets.Frontiers in immunology · 2020Article
- Article
- CD24Immune network · 2019Article
- T Cell Receptor Expression Timing and Signal Strength in the Functional Differentiation of Invariant Natural Killer T Cells.Frontiers in immunology · 2019Review
- Article
- Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17.World journal of diabetes · 2018Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Invariant natural killer T (iNKT) cells recognize glycolipids as antigens and diversify into NKT1 (IFN-γ), NKT2 (IL-4), and NKT17 (IL-17) functional subsets while developing in the thymus. Mechanisms that govern the balance between these functional subsets are poorly understood due, partly, to the lack of distinguishing surface markers. Here we identify the heparan sulfate proteoglycan syndecan-1 (sdc1) as a specific marker of naïve thymic NKT17 cells in mice and show that sdc1 deficiency significantly increases thymic NKT17 cells at the expense of NKT1 cells, leading to impaired iNKT cell-derived IFN-γ, both in vitro and in vivo. Using surface expression of sdc1 to identify NKT17 cells, we confirm differential tissue localization and interstrain variability of NKT17 cells, and reveal that NKT17 cells express high levels of TCR-β, preferentially use Vβ8, and are more highly sensitive to ɑ-GalCer than to CD3/CD28 stimulation. These findings provide a novel, noninvasive, simple method for identification, and viable sorting of naïve NKT17 cells from unmanipulated mice, and suggest that sdc1 expression negatively regulates homeostasis in iNKT cells. In addition, these findings lay the groundwork for investigating the mechanisms by which sdc1 regulates NKT17 cells.
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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.