ArticleBlood2015
Type II NKT-TFH cells against Gaucher lipids regulate B-cell immunity and inflammation.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- Value of Glucosylsphingosine (Lyso-Gb1) as a Biomarker in Gaucher Disease: A Systematic Literature Review.International journal of molecular sciences · 2020Pooled it
- Clinical outcomes after 4.5 years of eliglustat therapy for Gaucher disease type 1: Phase 3 ENGAGE trial final results.American journal of hematology · 2021Trial
- Outcomes after 8 years of eliglustat therapy for Gaucher disease type 1: Final results from the Phase 2 trial.American journal of hematology · 2019Trial
- Outcomes after 18 months of eliglustat therapy in treatment-naïve adults with Gaucher disease type 1: The phase 3 ENGAGE trial.American journal of hematology · 2017Trial
- Cumulative Antigen Suppression Reduces Clonal Plasma Cell Evolution in Gaucher Disease.American journal of hematology · 2026Article
- Rare Diseases as Engines of Biomedical Innovation: Lessons for Gene Therapy and Common Disease.The Yale journal of biology and medicine · 2026Review
- Gaucher disease: the hematologist's perspective of a multisystemic disorder.Annals of hematology · 2026Review
- The dual impact of GBA1 in disease: from germline mutations in neurological disorders to alterations in cancer.Cell death discovery · 2026Review
- Glucosylsphingosine (Lyso-Gb1): An Update on Its Use as a Biomarker in Gaucher Disease.International journal of molecular sciences · 2026Review
- Refining Mouse Models of Gaucher Disease: Advancing Mechanistic Insights, Biomarker Discovery, and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- T cells in cancer: mechanistic insights and therapeutic advances.Biomarker research · 2025Review
- Natural history of inflammation and impaired autophagy in children with Gaucher disease identified by newborn screening.Molecular genetics and metabolism reports · 2025Article
- Eliglustat substrate reduction therapy in children with Gaucher disease type 1.Frontiers in pediatrics · 2025Article
- Precision genomic profiling in Gaucher disease: insights from atypical presentations.Frontiers in genetics · 2025Article
- Immune cells: the key mediator between the gut microbiota and osteoporosis.Frontiers in immunology · 2025Review
- Case Report: Diagnosis of Gaucher disease in a toddler with acute respiratory failure.Frontiers in pediatrics · 2025Article
- Analysis of smoldering multiple myeloma according to the target of the monoclonal immunoglobulin of patients.HemaSphere · 2024Article
- Glycolipids in Parkinson's disease: beyond neuronal function.FEBS open bio · 2023Review
- MAITs and their mates: "Innate-like" behaviors in conventional and unconventional T cells.Clinical and experimental immunology · 2023Article
- Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic inflammation including B-cell activation is commonly observed in both inherited (Gaucher disease [GD]) and acquired disorders of lipid metabolism. However, the cellular mechanisms underlying B-cell activation in these settings remain to be elucidated. Here, we report that β-glucosylceramide 22:0 (βGL1-22) and glucosylsphingosine (LGL1), 2 major sphingolipids accumulated in GD, can be recognized by a distinct subset of CD1d-restricted human and murine type II natural killer T (NKT) cells. Human βGL1-22- and LGL1-reactive CD1d tetramer-positive T cells have a distinct T-cell receptor usage and genomic and cytokine profiles compared with the classical type I NKT cells. In contrast to type I NKT cells, βGL1-22- and LGL1-specific NKT cells constitutively express T-follicular helper (TFH) phenotype. Injection of these lipids leads to an increase in respective lipid-specific type II NKT cells in vivo and downstream induction of germinal center B cells, hypergammaglobulinemia, and production of antilipid antibodies. Human βGL1-22- and LGL1-specific NKT cells can provide efficient cognate help to B cells in vitro. Frequency of LGL1-specific T cells in GD mouse models and patients correlates with disease activity and therapeutic response. Our studies identify a novel type II NKT-mediated pathway for glucosphingolipid-mediated dysregulation of humoral immunity and increased risk of B-cell malignancy observed in metabolic lipid disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.