Evidence map›Paper›PMID 27563173›Full record

ArticleMediators of inflammation2016

TLR2-Dependent Signaling for IL-15 Production Is Essential for the Homeostasis of Intestinal Intraepithelial Lymphocytes.

Yuan Qiu, Aimin Pu, Hong Zheng, Minqiang Liu, Weigang Chen, Wensheng Wang, Weidong Xiao, Hua Yang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. 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
1.2field-weighted citation impact, top 21% 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, 24 citations in OpenAlex.

  1. Review
  2. Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026
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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

8 authors at 1 institution in 1 country.

Yuan QiuDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.
Aimin PuDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.
Hong ZhengDepartment of Thoracic Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.ORCID 0000-0003-3725-4541
Minqiang LiuDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.
Weigang ChenDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.
Wensheng WangDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.
Weidong XiaoDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.ORCID 0000-0002-6192-5344
Hua YangDepartment of General Surgery of Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing 400037, China.ORCID 0000-0002-8882-3436
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLR2 signaling is related to colitis and involved in regulation of innate immunity in the intestinal tract, but the mechanisms remain unclear. The aim of this study is to investigate how TLR2 affects differentiation of intraepithelial lymphocytes (IELs) and regulates the susceptibility of colitis. IELs were isolated from the small intestine and colon of mice, respectively. The IEL phenotype, activation, and apoptosis were examined using flow cytometry and RT-PCR. IL-15 expression and IEL location were detected through immunohistochemistry. The experimental colitis was induced by administration of dextran sulfate sodium (DSS). We found that the numbers of CD8αα (+), CD8αβ (+), and TCRγδ (+) IELs were significantly decreased in TLR2-deficient mice and the residual IELs displayed reduced activation and proliferation and increased apoptosis, accompanied with impaired IL-15 expression by intestinal epithelial cells (IECs). Further study showed that TLR2 signaling maintained the expression of IL-15 in IEC via NF-κB activation. Moreover, TLR2-deficient mice were found to be more susceptible to DSS-induced colitis as shown by the increased severity of colitis. Our results demonstrate that IECs contribute to the maintenance of IELs at least partly via TLR2-dependent IL-15 production, which provides a clue that may link IECs to innate immune protection of the host via IELs.

Indexed as

AnimalsApoptosisCell Line, TumorCell ProliferationColitisDextran SulfateFlow CytometryHomeostasisHumansImmunohistochemistryInterleukin-15IntestinesLymphocytesMaleMiceMice, Inbred C57BLDextran SulfateInterleukin-15Tlr2 protein, mouseToll-Like Receptor 2

Identifiers

PMID27563173
PMCPMC4983668
OpenAlexW2497583443

What OpenQuestion holds

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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.