ArticleScientific reports2017
Endotoxin tolerance in mast cells, its consequences for IgE-mediated signalling, and the effects of BCL3 deficiency.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Shaping neutrophil morphology and function: the importance of a segmented nucleus.Nature reviews. Immunology · 2026Review
- Sleep disturbances and psychological factors as mediators between gastrointestinal symptoms and disease severity in chronic spontaneous urticaria.The World Allergy Organization journal · 2026Article
- The Dual Role of Gut Microbiota and Their Metabolites in Hepatocellular Carcinoma: A Context-Dependent Framework.Microorganisms · 2025Review
- [Research progress in gut microbiota and metabolism in the pathogenesis of chronic urticaria].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Gut microbiota facilitate chronic spontaneous urticaria.Nature communications · 2024Article
- Immunomodulatory contribution of mast cells to the regenerative biomaterial microenvironment.NPJ Regenerative medicine · 2023Article
- LPS Guides Distinct Patterns of Training and Tolerance in Mast Cells.Frontiers in immunology · 2022Article
- Review
- Microglial-specific depletion of TAK1 is neuroprotective in the acute phase after ischemic stroke.Journal of molecular medicine (Berlin, Germany) · 2020Article
- The Role of Microbiota in Neutrophil Regulation and Adaptation in Newborns.Frontiers in immunology · 2020Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulation with lipopolysaccharide (LPS; endotoxin) not only causes rapid production of proinflammatory cytokines, but also induces a state of LPS hypo-responsiveness to a second LPS stimulation (endotoxin tolerance (ET)). Murine bone marrow-derived MCs (BMMCs) and peritoneal MCs (PMCs) developed ET as shown by an abrogated production of Il6/Tnf RNAs and IL-6/TNF-α proteins. In naive BMMCs, LPS stimulation induced a transient decline in the trimethylation of lysine 9 of the core histone H3 (H3K9me3), a suppressive chromatin mark, at the Il6/Tnf promoters, which correlated with p50(NFκB) and p65(NFκB) binding. Both demethylation and NFκB binding were abrogated in tolerant cells. In addition, cytosolic NFκB activation was suppressed in tolerant BMMCs. Intriguingly, antigen stimulation of naive and tolerant MCs induced comparable production of Il6/Tnf and IL-6/TNF-α, although ET also affected antigen-triggered activation of NFκB; pharmacological analysis indicated the importance of Ca
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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.