ArticleJournal of immunology (Baltimore, Md. : 1950)2008
A phosphatidylserine species inhibits a range of TLR- but not IL-1beta-induced inflammatory responses by disruption of membrane microdomains.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanisms of Immune Evasion, Dissemination, and Persistence in Leishmania amazonensis Infection.Parasite immunology · 2026Review
- Celery seed derived reconstituted lipid nanoparticles as an innate neuron-targeted neuroprotective nanomedicine for ischemic stroke treatment.Journal of nanobiotechnology · 2025Article
- In Vitro Effects of 5-Lipoxygenase Pathway Inhibition on Rhinovirus-Associated Bronchial Epithelial Inflammation.Pulmonary therapy · 2021Article
- TRAF3-interacting JNK-activating modulator promotes inflammation by stimulating translocation of Toll-like receptor 4 to lipid rafts.The Journal of biological chemistry · 2019Article
- DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling.Journal of virology · 2019Article
- Airway Epithelial Cells Generate Pro-inflammatory Tenascin-C and Small Extracellular Vesicles in Response to TLR3 Stimuli and Rhinovirus Infection.Frontiers in immunology · 2019Article
- Lipid raft localization of TLR2 and its co-receptors is independent of membrane lipid composition.PeerJ · 2018Article
- The θ-defensin retrocyclin 101 inhibits TLR4- and TLR2-dependent signaling and protects mice against influenza infection.Journal of leukocyte biology · 2017Article
- Human rhinovirus-induced inflammatory responses are inhibited by phosphatidylserine containing liposomes.Mucosal immunology · 2016Article
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- Roles of neutrophils in the regulation of the extent of human inflammation through delivery of IL-1 and clearance of chemokines.Journal of leukocyte biology · 2013Article
- Pellino-1 selectively regulates epithelial cell responses to rhinovirus.Journal of virology · 2012Article
- Interleukin-1β regulates CXCL8 release and influences disease outcome in response to Streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages.Infection and immunity · 2012Article
- Granulocytes in helminth infection -- who is calling the shots?Current medicinal chemistry · 2012Review
- Role of interleukin-1 and MyD88-dependent signaling in rhinovirus infection.Journal of virology · 2011Article
- Diesel exhaust particles override natural injury-limiting pathways in the lung.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- A central role for monocytes in Toll-like receptor-mediated activation of the vasculature.Immunology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
Abstract
TLRs detect conserved molecular patterns that are unique to microbes, enabling tailored responses to invading pathogens and modulating a multitude of immunopathological conditions. We investigated the ability of a naturally occurring stearoyl-arachidonoyl form of phosphatidylserine (SAPS) to inhibit the proinflammatory effects of TLR agonists in models of inflammation investigating the interaction of leukocytes with epithelial and endothelial cells. The responses to LPS of both epithelial and endothelial cells were highly amplified in the presence of PBMCs. Coincubation with SAPS markedly inhibited activation of cocultures by LPS, principally through inhibition of the TLR4 signaling pathway in PBMCs; however, this was not through downmodulation of TLR4 or coreceptor expression, nor was IL-1beta-induced cytokine release affected. SAPS also impaired Pam(3)CSK(4) (TLR2/1), Gardiquimod (TLR7/8), and Streptococcus pneumoniae-induced cytokine release, but had only modest effects on poly(I:C) (TLR3)-induced responses. Fluorescence resonance energy transfer analysis of molecular associations revealed that SAPS disrupted the association of both TLR4 and TLR2 with their respective membrane partners that are required for signaling. Thus, our data reinforce the existence and importance of cooperative networks of TLRs, tissue cells, and leukocytes in mediating innate immunity, and identify a novel disrupter of membrane microdomains, revealing the dependence of TLR signaling on localization within these domains.
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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.