ArticleThe Journal of experimental medicine1999
Endotoxin-tolerant mice have mutations in Toll-like receptor 4 (Tlr4)
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 426 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.
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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
426 citing papers in PubMed, 1,535 citations in OpenAlex.
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- Microbial and metabolic signatures of humanized microbiome mice associate withFrontiers in immunology · 2026Article
- TLR4 competence and mouse models of sublethal leptospirosis.PLoS neglected tropical diseases · 2025Article
- Vibrio cholerae cytolysin induces pro-inflammatory and death signals through novel TLR assembly.PLoS pathogens · 2025Article
- Natural genetic variation in wild-derived mice controls host survival and transcriptional responses during endotoxic shock.ImmunoHorizons · 2025Article
- Gut microbiota is involved in the exacerbation of adrenal glucocorticoid steroidogenesis in diabetic animals by activation of the TLR4 pathway.Frontiers in endocrinology · 2025Article
- The influence of sex on neuroimmune communication, pain, and physiology.Biology of sex differences · 2024Review
- Lovastatin Combination Therapy Increases the Survival and Proliferation of Rat Bone Marrow-Derived Mesenchymal Stem Cells Against the Inflammatory Activity of Lipopolysaccharide.Cell biochemistry and biophysics · 2024Article
- Origin recognition complex subunit 6 (ORC6) is a key mediator of LPS-induced NFκB activation and the pro-inflammatory response.Cell communication and signaling : CCS · 2024Article
- Blood-brain barrier alterations and their impact on Parkinson's disease pathogenesis and therapy.Translational neurodegeneration · 2024Review
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
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- Serum soluble toll-like receptor 4 and risk for clinical severity in COVID-19 patients.Pneumonia (Nathan Qld.) · 2024Article
- The translational value of calcium pyrophosphate deposition disease experimental mouse models.Frontiers in medicine · 2024Review
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- Small molecule modulators of immune pattern recognition receptors.RSC chemical biology · 2023Review
366 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial lipopolysaccharide (LPS) provokes a vigorous, generalized proinflammatory state in the infected host. Genetic regulation of this response has been localized to the Lps locus on mouse chromosome 4, through study of the C3H/HeJ and C57BL/10ScCr inbred strains. Both C3H/HeJ and C57BL/10ScCr mice are homozygous for a mutant Lps allele (Lpsd/d) that confers hyporesponsiveness to LPS challenge, and therefore exhibit natural tolerance to its lethal effects. Genetic and physical mapping of 1,345 backcross progeny segregating this mutant phenotype confined Lps to a 0.9-cM interval spanning 1.7 Mb. Three transcription units were identified within the candidate interval, including Toll-like receptor 4 (Tlr4), part of a protein family with members that have been implicated in LPS-induced cell signaling. C3H/HeJ mice have a point mutation within the coding region of the Tlr4 gene, resulting in a nonconservative substitution of a highly conserved proline by histidine at codon 712, whereas C57BL/ 10ScCr mice exhibit a deletion of Tlr4. Identification of distinct mutations involving the same gene at the Lps locus in two different hyporesponsive inbred mouse strains strongly supports the hypothesis that altered Tlr4 function is responsible for endotoxin tolerance.
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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.