Evidence map›Paper›PMID 31018808›Full record

ArticleInnate immunity2019

Expression of TLR2, TLR3, TLR4, and TLR7 on pulmonary lymphocytes of Schistosoma japonicum-infected C57BL/6 mice.

Dianhui Chen, Yi Zhao, Yuanfa Feng, Chenxi Jin, Quan Yang, Huaina Qiu, Hongyan Xie, Sihao Xie, Yi Zhou, Jun Huang

Open access · goldAbstract read
In one paragraph

Article in Innate immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  13. Changes of CD103-expressing pulmonary CD4BMC infectious diseases · 2019
    Article
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

10 authors at 1 institution in 1 country.

Dianhui Chen1 The Affiliated Brain Hospital of Guangzhou Medical University (Guangzhou Huiai Hospital), Guangzhou Medical University, China.ORCID 0000-0002-9471-6426
Yi Zhao2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Yuanfa Feng2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Chenxi Jin2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Quan Yang2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Huaina Qiu2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Hongyan Xie2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Sihao Xie2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Yi Zhou3 College of Pharmacy, Guangzhou Medical University, China.
Jun Huang2 Sino-French Hoffmann Institute, School of Basic Medical Sciences and Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, China.
Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the paramount role of TLRs in the induction of innate immune and inflammatory responses, there is a paucity of studies on the role of TLRs in Schistosoma japonicum infection. Here, we observed obvious infiltration of inflammatory cells in S. japonicum-infected C57BL/6 mouse lungs. Expression and release of IFN-γ, IL-4, and IL-17 were significantly higher in pulmonary lymphocytes from infected mice compared with control mice in response to anti-CD3 plus anti-CD28 mAbs. Higher percentages of TLR2, TLR3, TLR4, and TLR7 were expressed on such lymphocytes, and the TLR agonists PGN, Poly I:C, LPS, and R848 induced a higher level of IFN-γ. However, a higher level of IL-4 was found in the supernatant of pulmonary lymphocytes from infected mice stimulated by these TLR agonists plus CD3 Ab. Only R848 plus anti-CD3 mAb could induce a higher level of IFN-γ in such lymphocytes. TLR expressions were then compared on different pulmonary lymphocytes after infection, including T cells, B cells, NK cells, NKT cells, and γδT cells. The expression levels of TLR3 on T cells, B cells, NK cells, and γδT cells were increased in the lungs after infection. NK cells also expressed higher levels of TLR4 after infection of control mice. Collectively, these findings highlight the potential role of TLR expression in the context of S. japonicum infection.

Indexed as

AnimalsFemaleGene Expression RegulationHumansInterferon-gammaInterleukin-4LungLymphocytesMembrane GlycoproteinsMiceMice, Inbred C57BLParasite Egg CountSchistosoma japonicumSchistosomiasis japonicaToll-Like Receptor 2Toll-Like Receptor 3Interferon-gammaInterleukin-4Membrane GlycoproteinsTlr2 protein, mouseTLR3 protein, mouseTlr4 protein, mouseTlr7 protein, mouseToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 7cytokinesligandslungTLRs

Identifiers

PMID31018808
PMCPMC6830883
OpenAlexW2941327646

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.