ArticleImmunology2007
Role of endogenous 4-1BB in the development of systemic lupus erythematosus.
Article in Immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- CD137 agonists in mice suppress germinal center responses by increasing the immunosuppressive activity of follicular regulatory T-cells.The EMBO journal · 2026Article
- Discovery of core genes for systemic lupus erythematosus via genome-wide aggregated trans-effects analysis.Genes and immunity · 2025Article
- Clinical and functional characterization of a novelFrontiers in immunology · 2025Article
- LIGHT regulated gene expression in rheumatoid synovial fibroblasts.Molecular biology reports · 2024Article
- 4-1BB immunotherapy: advances and hurdles.Experimental & molecular medicine · 2024Review
- Membrane and Soluble CD137 in Systemic Lupus Erythematosus: Role as Biomarkers for Disease Activity.Journal of immunology research · 2023Article
- 4-1BB: A promising target for cancer immunotherapy.Frontiers in oncology · 2022Review
- Regulatory T Cells Inhibit T Cell Activity by Downregulating CD137 Ligand via CD137 Trogocytosis.Cells · 2021Article
- The Murine CD137/CD137 Ligand Signalosome: A Signal Platform Generating Signal Complexity.Frontiers in immunology · 2020Review
- Article
- Review
- The Progress of Investigating the CD137-CD137L Axis as a Potential Target for Systemic Lupus Erythematosus.Cells · 2019Review
- Deletion of CD137 Ligand Exacerbates Renal and Cutaneous but Alleviates Cerebral Manifestations in Lupus.Frontiers in immunology · 2019Article
- A comprehensive review on the role of co-signaling receptors and Treg homeostasis in autoimmunity and tumor immunity.Journal of autoimmunity · 2018Review
- Overcoming Tumor-Induced Immune Suppression: From Relieving Inhibition to Providing Costimulation with T Cell Agonists.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2018Review
- Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- Co-stimulatory and Co-inhibitory Pathways in Autoimmunity.Immunity · 2016Review
- CD137 and CD137L signals are main drivers of type 1, cell-mediated immune responses.Oncoimmunology · 2016Review
- 4-1BB Agonists: Multi-Potent Potentiators of Tumor Immunity.Frontiers in oncology · 2015Review
- Targeting dendritic cell function during systemic autoimmunity to restore tolerance.International journal of molecular sciences · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is characterized by the production of autoantibodies directed against nuclear antigens including nucleosomes and DNA. To determine the role of T-cell costimulatory molecule 4-1BB in the regulation of SLE, MRL-Fas(lpr) (lpr) mice deficient in 4-1BB (lpr/4-1BB(-/-)) were generated and their disease phenotype was compared to that of control lpr mice. The main finding of this study is that the lpr/4-1BB(-/-) mice had more pronounced skin lesions which appeared earlier, increased lymphadenopathy, increased renal damage, and higher mortality than 4-1BB-intact control lpr mice. The increased severity of lesions in lpr/4-1BB(-/-) mice was closely associated with increases in CD4(+) T, CD3(+) B220(+) double-negative T cells, serum immunoglobulin, anti-dsDNA autoantibodies, and tissue immunoglobulin deposits. These data suggest that the 4-1BB-4-1BB ligand signalling pathway plays an important role in SLE and that deletion of 4-1BB confers susceptibility to lpr mice, leading to accelerated induction of disease and early mortality.
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.