ArticleNature genetics2008
Polymorphism at the TNF superfamily gene TNFSF4 confers susceptibility to systemic lupus erythematosus.
Article in Nature genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 5 of them syntheses that pooled it.
What it found
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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
121 citing papers in PubMed, 5 syntheses or guidelines pooled it, 219 citations in OpenAlex.
- Trans-ancestry, Bayesian meta-analysis discovers 20 novel risk loci for inflammatory bowel disease in an African American, East Asian and European cohort.Human molecular genetics · 2023Pooled it
- TNFSF4 is a risk factor to systemic lupus erythematosus in a Latin American population.Clinical rheumatology · 2021Pooled it
- Meta-analysis of two Chinese populations identifies an autoimmune disease risk allele in 22q11.21 as associated with systemic lupus erythematosus.Arthritis research & therapy · 2015Pooled it
- Independent replication and meta analysis of association studies establish TNFSF4 as a susceptibility gene preferentially associated with the subset of anticentromere-positive patients with systemic sclerosis.The Journal of rheumatology · 2012Pooled it
- Association of EBF1, FAM167A(C8orf13)-BLK and TNFSF4 gene variants with primary Sjögren's syndrome.Genes and immunity · 2011Pooled it
- Association of OX40L polymorphisms with sporadic breast cancer in northeast Chinese Han population.PloS one · 2012Trial
- Dynamic cellular programs of human cardiac allograft rejection revealed by spatial transcriptomics.Nature cardiovascular research · 2026Article
- Genomic Landscape of Systemic Lupus Erythematosus and Lupus Nephritis Globally and the Gaps in Africa.International journal of molecular sciences · 2026Review
- Article
- Association between OX40L rs1234314 and rs844648 polymorphisms and unexplained recurrent pregnancy loss.Molecular biology reports · 2025Article
- Deciphering the Population Characteristics of Leiqiong Cattle Using Whole-Genome Sequencing Data.Animals : an open access journal from MDPI · 2025Article
- Human OX40L-CAR-TScience translational medicine · 2024Article
- Evolving understanding of autoimmune mechanisms and new therapeutic strategies of autoimmune disorders.Signal transduction and targeted therapy · 2024Review
- Association ofHeliyon · 2024Article
- TNF superfamily control of tissue remodeling and fibrosis.Frontiers in immunology · 2023Review
- Multi-omics integrative analysis reveals the role of tumor necrosis factor superfamily member 4 in keloidal scarring.American journal of translational research · 2023Article
- Activation Markers on B and T Cells and Immune Checkpoints in Autoimmune Rheumatic Diseases.International journal of molecular sciences · 2022Review
- T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022Review
- Understanding the Concept of Pre-Clinical Autoimmunity: Prediction and Prevention of Systemic Lupus Erythematosus: Identifying Risk Factors and Developing Strategies Against Disease Development.Frontiers in immunology · 2022Review
- Sauchinone alleviates dextran sulfate sodium-induced ulcerative colitisFrontiers in microbiology · 2022Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a multisystem complex autoimmune disease of uncertain etiology (OMIM 152700). Over recent years a genetic component to SLE susceptibility has been established. Recent successes with association studies in SLE have identified genes including IRF5 (refs. 4,5) and FCGR3B. Two tumor necrosis factor (TNF) superfamily members located within intervals showing genetic linkage with SLE are TNFSF4 (also known as OX40L; 1q25), which is expressed on activated antigen-presenting cells (APCs) and vascular endothelial cells, and also its unique receptor, TNFRSF4 (also known as OX40; 1p36), which is primarily expressed on activated CD4+ T cells. TNFSF4 produces a potent co-stimulatory signal for activated CD4+ T cells after engagement of TNFRSF4 (ref. 11). Using both a family-based and a case-control study design, we show that the upstream region of TNFSF4 contains a single risk haplotype for SLE, which is correlated with increased expression of both cell-surface TNFSF4 and the TNFSF4 transcript. We hypothesize that increased expression of TNFSF4 predisposes to SLE either by quantitatively augmenting T cell-APC interaction or by influencing the functional consequences of T cell activation via TNFRSF4.
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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.