Evidence map›Paper›PMID 28949386›Full record

ArticleInternational journal of molecular medicine2017

TIM4-TIM1 interaction modulates Th2 pattern inflammation through enhancing SIRT1 expression.

Tianyong Hu, Xiaoqin Fan, Li Ma, Jiangqi Liu, Yunli Chang, Pingchang Yang, Shuqi Qiu, Tao Chen, Litao Yang, Zhiqiang Liu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. 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 22% 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, 25 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Tianyong HuImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Xiaoqin FanImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Li MaImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Jiangqi LiuImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Yunli ChangDepartment of Gastroenterology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 201318, P.R. China.
Pingchang YangShenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, Guangdong 518060, P.R. China.
Shuqi QiuImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Tao ChenImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Litao YangImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Zhiqiang LiuImmunology and Allergy Laboratory, Longgang ENT Hospital, Institute of ENT and Shenzhen Key Laboratory of ENT, Shenzhen, Guangdong 518172, P.R. China.
Longgang Central Hospital · CNPudong New Area People's Hospital · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skewed T helper 2 (Th2)‑cell polarization plays a critical role in the pathogenesis of allergic inflammations; however, the underlying mechanisms require further elucidation. The aim of the present study was to investigate the mechanisms through which the interaction between T‑cell immunoglobulin and mucin domain (TIM)4 and TIM1 regulates the expression of silent information regulator 1 (SIRT1) in Th2 cells, and the role of SIRT1 in Th2‑cell polarization during nasal allergic inflammation. The results demonstrated that TIM4 expression by splenic dendritic cells was increased in mice with allergic rhinitis, and the TIM4̸TIM1 interaction promoted CD4+ T cells to express SIRT1 during allergic inflammation via enhancing phosphoinositide 3‑kinase/Akt phosphorylation. SIRT1 then facilitated CD4+ T‑cell proliferation through downregulating the expression of Fas ligand, caspase-3 and p53 in mice with nasal allergic inflammation. In conclusion, the interaction of TIM4̸TIM1 was found to promote Th2‑cell proliferation through enhancing SIRT1 expression in mice with nasal allergic rhinitis.

Indexed as

Gene Expression RegulationAnimalsBiomarkersDisease Models, AnimalFemaleGene SilencingHepatitis A Virus Cellular Receptor 1InflammationMembrane ProteinsMiceProtein BindingRhinitis, AllergicSirtuin 1Th2 CellsBiomarkersHAVCR1 protein, humanHepatitis A Virus Cellular Receptor 1Membrane ProteinsSIRT1 protein, humanSirtuin 1TIMD4 protein, human

Identifiers

PMID28949386
PMCPMC5627870
OpenAlexW2759954893

What OpenQuestion holds

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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.