ReviewMolecules and cells2012
Reverse signaling through the co-stimulatory ligand, CD137L, as a critical mediator of sterile inflammation.
Review in Molecules and cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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
10 citing papers in PubMed, 21 citations in OpenAlex.
- Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke.Frontiers in immunology · 2026Review
- TNFSF9 Silence Impedes Cerebral Ischemia-Reperfusion Injury via Modulating SLC3A2 Expression in Brain Microvascular Endothelial Cells.Journal of molecular neuroscience : MN · 2025Article
- Article
- Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19.Nature communications · 2023Article
- Contributions of Costimulatory Molecule CD137 in Endothelial Cells.Journal of the American Heart Association · 2021Review
- Deciphering molecular properties of hypermutated gastrointestinal cancer.Journal of cellular and molecular medicine · 2019Article
- Blocking the 4-1BB Pathway Ameliorates Crystalline Silica-induced Lung Inflammation and Fibrosis in Mice.Theranostics · 2016Article
- HITS-CLIP analysis uncovers a link between the Kaposi's sarcoma-associated herpesvirus ORF57 protein and host pre-mRNA metabolism.PLoS pathogens · 2015Article
- Involvement of CD137 ligand signaling in neural stem cell death.Molecules and cells · 2013Article
- Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand.Immune network · 2012Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD137 (also called 4-1BB and TNFRSF9) has recently received attention as a therapeutic target for cancer and a variety of autoimmune and inflammatory diseases. Stimulating CD137 in vivo enhances CD8(+) T cell-activity and results in strong immunosuppression in some contexts. This paradoxical phenomenon may be partially explained by the ability of CD137-stimulating reagents (usually agonistic monoclonal antibodies against CD137) to overactivate T cells and other CD137-expressing cells. This over-activity is associated with deleting pathogenic T cells and B cells or generating a tolerogenic microenvironment. Recent studies, however, suggest that the biology of CD137 and its ligand (CD137L) are more complex, mainly due to bidirectional signaling between CD137 and CD137L. For example, signaling through CD137L in non-hematopoietic cells such as epithelial cells and endothelial cells has been shown to play an essential role in sterile inflammation by regulating immune cell recruitment. One outstanding, and clinically important, issue is understanding how bidirectional signaling through CD137 and CD137L controls the vicious cycle of sterile inflammation (e.g., ischemia-reperfusion tissue injury and meta-inflammatory diseases).
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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.