ArticleProceedings of the National Academy of Sciences of the United States of America2013
Modulating the innate immune response by combinatorial engineering of endotoxin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 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
155 citing papers in PubMed, 226 citations in OpenAlex.
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- The bug, the burden, and the biology: beyond host-centric phenotyping in sepsis.The Journal of clinical investigation · 2026Article
- Designing and immuno-informatics evaluation of a multi-epitope vaccine targeting lipoprotein A-4'-phosphatase (LpxF) forFrontiers in bioinformatics · 2026Article
- Endotoxin Tolerance Impinges on T Cell Activation and Chemoattraction in Autoimmune Diabetes.Journal of immunology research · 2026Article
- Advances in microbial extracellular vesicles: synthetic biology platforms and medical applications.Extracellular vesicles and circulating nucleic acids · 2026Review
- Potentiality of LPS in Ameliorating the Histopathological Responses in Visceral Leishmaniasis-Infected Mice.Journal of parasitology research · 2026Article
- Engineering low-endotoxin lipid A in a double auxotrophFrontiers in cellular and infection microbiology · 2026Article
- Commensal bacterial glycosylation at the interface of host-bacteria interactions.Gut microbes · 2025Review
- Mechanistic basis of antimicrobial resistance mediated by the phosphoethanolamine transferase MCR-1.Nature communications · 2025Article
- Lipid A mimetic BECC438 potentiates durable and balanced antibody responses in an ovalbumin murine model of vaccination.ImmunoHorizons · 2025Article
- Bioengineering Outer-Membrane Vesicles for Vaccine Development: Strategies, Advances, and Perspectives.Vaccines · 2025Review
- Structural insight into TLR4/MD-2 activation by synthetic LPS mimetics with distinct binding modes.Nature communications · 2025Article
- Beyond the Toll-Like Receptor 4. Structure-Dependent Lipopolysaccharide Recognition Systems: How far are we?ChemMedChem · 2025Review
- Stability of cytokine, cellular and clinical response to the intravenous LPS challenge repeated after one year: a healthy volunteer trial.Medical microbiology and immunology · 2025Article
- β-Barrel proteins dictate the effect of core oligosaccharide composition on outer membrane mechanics.Biophysical journal · 2025Article
- Review on bacterial outer membrane vesicles: structure, vesicle formation, separation and biotechnological applications.Microbial cell factories · 2025Review
- Opportunities and challenges of bacterial extracellular vesicles in regenerative medicine.Journal of nanobiotechnology · 2025Review
95 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
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Despite its highly inflammatory nature, LPS is a molecule with remarkable therapeutic potential. Lipid A is a glycolipid that serves as the hydrophobic anchor of LPS and constitutes a potent ligand of the Toll-like receptor (TLR)4/myeloid differentiation factor 2 receptor of the innate immune system. A less toxic mixture of monophosphorylated lipid A species (MPL) recently became the first new Food and Drug Administration-approved adjuvant in over 70 y. Whereas wild-type Escherichia coli LPS provokes strong inflammatory MyD88 (myeloid differentiation primary response gene 88)-mediated TLR4 signaling, MPL preferentially induces less inflammatory TRIF (TIR-domain-containing adaptor-inducing IFN-β)-mediated responses. Here, we developed a system for combinatorial structural diversification of E. coli lipid A, yielding a spectrum of bioactive variants that display distinct TLR4 agonist activities and cytokine induction. Mice immunized with engineered lipid A/antigen emulsions exhibited robust IgG titers, indicating the efficacy of these molecules as adjuvants. This approach demonstrates how combinatorial engineering of lipid A can be exploited to generate a spectrum of immunostimulatory molecules for vaccine and therapeutics development.
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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.