ArticleIranian biomedical journal2016
Activation of Toll-Like Receptors 2 by High-Mobility Group Box 1 in Monocytes from Patients with Ischemic Stroke.
Article in Iranian biomedical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 6 citations in OpenAlex.
- Research on the innate immune response in transgenic mice following ischemic stroke.Frontiers in aging neuroscience · 2024Review
- Neuroinflammation: friend and foe for ischemic stroke.Journal of neuroinflammation · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStroke is a leading cause of death all around the world, and ischemic stroke is considered to be the most common stroke type. Toll-like receptors (TLRs) are important molecules for detection of both pathogen invasion and tissue damage. In this regard, the purpose of this study was to assess the expression level of TLR2 on monocytes in patients with ischemic stroke and to evaluate the expression change profile following high-mobility group box 1 (HMGB1) stimulation.
methodsA total of 30 patients with ischemic stroke were enrolled from November 2013 to September 2014. The real-time PCR and ELISA assays were applied to detect the concentrations of TLR2 mRNAs.
resultsTLR2 expression was found to be increased in patients with ischemic stroke, as compared to the healthy control group (P<0.001). Also, anti-TLR2 antibodies were able to decrease the expression levels of IL-17, IL-6 and IL-33. This result implies that the enhanced TLR2 pathway and Th17 cell polarization may be due to HMGB1 stimulation in ischemic stroke.
conclusionFurther clinical studies are needed for development of a new treatment strategy to inhibit the HMGB1 pathway, thus preventing the inflammation in ischemic stroke patients.
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Registered trials
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