ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2017
Advanced glycation endproducts induce self- and cross-tolerance in monocytes.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.Frontiers in immunology · 2026Article
- Delayed Immune Response Upon Injury in Diabetic Wounds Impedes Healing.Immunity, inflammation and disease · 2025Article
- A Role for Advanced Glycation End Products in Molecular Ageing.International journal of molecular sciences · 2023Review
- Article
- The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAdvanced glycation endproducts (AGEs) are well-known inflammatory mediators, which are recognized by immune cells through their corresponding receptor RAGE and have been shown to participate in the pathophysiology of a variety of acute as well as chronic inflammatory diseases. Nevertheless, no data are available on the aftermath of AGE recognition on immune cells. MATERIALS AND
methodsWe used the monocytic cell line MonoMac6 as well as primary human monocytes for double stimulation experiments. We measured secreted as well as intracellular levels of TNF-α using ELISA and flow cytometry. In addition, gene expression of surface receptors (RAGE and TLR4) and TNF were measured by qPCR.
resultsStimulation with AGE leads to a dose-dependent induction of self- and cross-tolerance in both primary monocytes as well as the MonoMac6 cell line. The AGE tolerance depended neither on a decreased expression of RAGE or TLR4, nor on a decrease of TNF-α expression. Nevertheless, intracellular TNF-α was decreased, hinting towards a posttranscriptional regulation.
conclusionHigh levels of AGEs are capable to activate immune cells at first, but induce a secondary state of hypo-responsiveness in these cells. Based on the origin of its causal agent, we propose this phenomenon to be "metabolic tolerance".
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