ArticleNature communications2017
Death receptor 6 contributes to autoimmunity in lupus-prone mice.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Identification and experimental validation of glycosylation related differentially expressed genes as diagnostic biomarkers in systemic lupus erythematosus.Scientific reports · 2025Article
- A structural atlas of death domain fold proteins reveals their versatile roles in biology and function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A proteomic map of thromboinflammatory signatures in antiphospholipid syndrome: results from antiphospholipid syndrome alliance for clinical trials and international networking (APS ACTION) registry.Frontiers in immunology · 2025Article
- Abnormally high expression of D1-like dopamine receptors on lupus CD4Lupus science & medicine · 2023Article
- Endothelial cell activation and glycocalyx shedding - potential as biomarkers in patients with lupus nephritis.Frontiers in immunology · 2023Review
- Nectin-2 Acts as a Viral Entry Mediated Molecule That Binds to Human Herpesvirus 6B Glycoprotein B.Viruses · 2022Article
- Bioactive borate glass triggers phenotypic changes in adipose stem cells.Journal of materials science. Materials in medicine · 2020Article
- Proapoptotic Mitochondrial Carrier Homolog Protein PSAP Mediates Death Receptor 6 Induced Apoptosis.Journal of Alzheimer's disease : JAD · 2020Article
- Disease Stage-Specific Pathogenicity of CD138 (Syndecan 1)-Expressing T Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2020Article
- Spatial and functional heterogeneity of follicular helper T cells in autoimmunity.Current opinion in immunology · 2019Review
- NrCAM is a marker for substrate-selective activation of ADAM10 in Alzheimer's disease.EMBO molecular medicine · 2019Article
- Three Novel Players: PTK2B, SYK, and TNFRSF21 Were Identified to Be Involved in the Regulation of Bovine Mastitis Susceptibility via GWAS and Post-transcriptional Analysis.Frontiers in immunology · 2019Article
- Non-cell-autonomous function of DR6 in Schwann cell proliferation.The EMBO journal · 2018Article
- Isolation and functional analysis of syndecans.Methods in cell biology · 2018Article
- Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective.Trends in molecular medicine · 2017Review
- Systemic lupus erythematosus: New pathway blocks disease in lupus-prone mice.Nature reviews. Rheumatology · 2017Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expansion of autoreactive follicular helper T (Tfh) cells is tightly restricted to prevent induction of autoantibody-dependent immunological diseases, such as systemic lupus erythematosus (SLE). Here we show expression of an orphan immune regulator, death receptor 6 (DR6/TNFRSF21), on a population of Tfh cells that are highly expanded in lupus-like disease progression in mice. Genome-wide screening reveals an interaction between syndecan-1 and DR6 resulting in immunosuppressive functions. Importantly, syndecan-1 is expressed specifically on autoreactive germinal centre (GC) B cells that are critical for maintenance of Tfh cells. Syndecan-1 expression level on GC B cells is associated with Tfh cell expansion and disease progression in lupus-prone mouse strains. In addition, Tfh cell suppression by DR6-specific monoclonal antibody delays disease progression in lupus-prone mice. These findings suggest that the DR6/syndecan-1 axis regulates aberrant GC reactions and could be a therapeutic target for autoimmune diseases such as SLE.
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.