ArticleNeuroimmunomodulation2014
Toll-like receptor 9 is required for chronic stress-induced immune suppression.
Article in Neuroimmunomodulation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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
8 citing papers in PubMed, 23 citations in OpenAlex.
- The crosstalk between nerves and immunity: chronic stress as a driver of tumor progression.Frontiers in immunology · 2026Review
- Review
- Activation of cell-free mtDNA-TLR9 signaling mediates chronic stress-induced social behavior deficits.Molecular psychiatry · 2023Article
- Effect of chronic stress on tumorigenesis and development.Cellular and molecular life sciences : CMLS · 2022Review
- Jujuboside B Reverse CUMS-Promoted Tumor Progression via Blocking PI3K/Akt and MAPK/ERK and Dephosphorylating CREB Signaling.Journal of immunology research · 2022Article
- Critical role of Tim-3 mediated autophagy in chronic stress induced immunosuppression.Cell & bioscience · 2019Article
- TGF-β1/Smad2/3/Foxp3 signaling is required for chronic stress-induced immune suppression.Journal of neuroimmunology · 2018Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectivesMental and physical stress can suppress the immune system in both humans and animals. The mechanism by which stress affects immune responses, however, remains poorly defined. Toll-like receptors (TLRs) play a key role in modulating immune responses and cell survival. The mechanisms by which TLRs modulate chronic stress are largely unexplored.
methodsSix- to 8-week-old male mice were subjected to chronic 12-hour daily physical restraint stress. Apoptotic cells were determined by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay. We examined cytokine levels by enzyme-linked immunosorbent Assay (ELISA). The expression of CYP11A1 was determined by quantitative real-time RT-PCR.
resultsTLR9-deficient mice were resistant to chronic stress-induced lymphocyte apoptosis. In addition, in TLR9 knockout (KO) mice, chronic stress-induced upregulation of corticosterone levels was significantly decreased. Notably, lymphocytes from both TLR9 KO and wild-type mice were similarly sensitive to corticosteroid-induced cell apoptosis. Moreover, TLR9 deficiency blocked the chronic stress-induced imbalance in T helper (Th) 1 and Th2 cytokine levels.
conclusionTaken together, our findings reveal that TLR9 plays an essential role in chronic stress-induced immune suppression.
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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.