Evidence map›Paper›PMID 36619523›Full record

ArticleFrontiers in pediatrics2022

Increased expression of the TLR7/9 signaling pathways in chronic active EBV infection.

Luyao Liu, Ying Wang, Wenjie Wang, Wenjing Ying, Bijun Sun, Xiaochuan Wang, Jinqiao Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. TLR2 and TLR9 in Brain Cancer Patients in Relation to EBV Status.International journal of molecular sciences · 2026
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  11. Serum TLR2 and TLR9 in Prostate Cancer Patients in Relation to EBV Status.International journal of molecular sciences · 2024
    Article
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  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Luyao LiuDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Ying WangDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Wenjie WangDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Wenjing YingDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Bijun SunDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Xiaochuan WangDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Jinqiao SunDepartment of Clinical Immunology, Children's Hospital of Fudan University, National Chlidren's Medical Center, Shanghai, China.
Children's Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to investigate the immunological mechanisms of the Toll-like receptor (TLR) signaling pathways in different types of Epstein-Barr virus (EBV) infection. We retrospectively summarized the clinical data, routine laboratory tests and the immunological function of the infectious mononucleosis (IM) and chronic active EBV infection (CAEBV) patients. A real-time quantitative PCR array was used to detect the mRNA expression levels of TLR7/TLR9 and myeloid-differentiation factor 88 (MyD88). Flow cytometry was used to detect the protein expression of TLR7/TLR9. The MyD88 and nuclear factor-κB (NF-κB) (p65) protein were detected by western blotting. A cytometric bead array (CBA) assay was used to detect the expression of downstream cytokines. CAEBV patients presented with increased expression of TLR7/TLR9 in monocytes and B lymphocytes. TLR9 expression in the B lymphocytes of IM patients was decreased compared with the CAEBV pateints. Downstream signaling mediators, including MyD88 and NF-κB, were revealed to be increased in EBV-infected patients. Moreover, the expression of MyD88 and NF-κB was higher in CAEBV patients, leading to disrupted balance of downstream cytokines. EBV may activate the immune system

Indexed as

chronic active EBV infectionepstein-Barr virusexcessive inflammatory responseimmune responsetoll-like receptor

Identifiers

PMID36619523
PMCPMC9811674
OpenAlexW4312071076

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.