ArticleEuropean journal of immunology2015
Inhibition of 4-1BBL-regulated TLR response in macrophages ameliorates endotoxin-induced sepsis in mice.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 17 citations in OpenAlex.
- Single-cell analysis reveals an important role of CD137L+ macrophages in the host response to uropathogenic Escherichia coli infection in the bladder.PLoS pathogens · 2025Article
- 4-1BB-4-1BBL cis-interaction contributes to the survival of self-reactive CD8Cellular & molecular immunology · 2023Article
- MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.Journal of immunology research · 2023Article
- Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases.Cellular and molecular life sciences : CMLS · 2022Review
- 4-1BBL Regulates the Polarization of Macrophages, and Inhibition of 4-1BBL Signaling Alleviates Imiquimod-Induced Psoriasis.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The Murine CD137/CD137 Ligand Signalosome: A Signal Platform Generating Signal Complexity.Frontiers in immunology · 2020Review
- Recent Advances in ADAM17 Research: A Promising Target for Cancer and Inflammation.Mediators of inflammation · 2017Review
- The neutrophil elastase inhibitor, sivelestat, attenuates sepsis-related kidney injury in rats.International journal of molecular medicine · 2016Article
- CD137 and CD137L signals are main drivers of type 1, cell-mediated immune responses.Oncoimmunology · 2016Review
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 3 institutions in 2 countries.
Funding
Abstract
Activation of Toll-like receptor (TLR) signaling rapidly induces the expression of inflammatory genes, which is persistent for a defined period of time. However, uncontrolled and excessive inflammation may lead to the development of diseases. 4-1BB ligand (4-1BBL) plays an essential role in sustaining the expression of inflammatory cytokines by interacting with TLRs during macrophage activation. Here, we show that inhibition of 4-1BBL signaling reduced the inflammatory responses in macrophages and ameliorated endotoxin-induced sepsis in mice. A 4-1BB-Fc fusion protein significantly reduced TNF production in macrophages by blocking the oligomerization of TLR4 and 4-1BBL. Administration of 4-1BB-Fc suppressed LPS-induced sepsis by reducing TNF production, and the coadministration of anti-TNF and 4-1BB-Fc provided better protection against LPS-induced sepsis. Taken together, these observations suggest that inhibition of the TLR/4-1BBL complex formation may be highly efficient in protecting against continued inflammation, and that 4-1BB-Fc could be a potential therapeutic target for the treatment of inflammatory diseases.
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.