Evidence map›Paper›PMID 30753412›Full record

ArticlePathogens and disease2019

Accumulation of EBI3 induced by virulent Mycobacterium tuberculosis inhibits apoptosis in murine macrophages.

Jia-Hui Deng, Han-Yu Chen, Chun Huang, Jia-Min Yan, Zhinan Yin, Xiao-Lian Zhang, Qin Pan

Open access · hybridAbstract read
In one paragraph

Article in Pathogens and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 15 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

7 authors at 2 institutions in 1 country.

Jia-Hui DengState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Han-Yu ChenState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Chun HuangState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Jia-Min YanState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Zhinan YinThe First Affiliated Hospital, Biomedical Translational Research Institute and School of Pharmacy, Jinan University, 601 Huangpu Rd, Guangzhou 510632, China.
Xiao-Lian ZhangState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Qin PanState Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Rd 185#, Wuhan 430071, China.
Wuhan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are the primary host target cells of Mycobacterium tuberculosis (M. tb). As a subunit of immunoregulatory cytokines IL-27 and IL-35, Epstein-Barr virus-induced gene 3 (EBI3) has typically been explored as the secreted form and assessed in terms of its effects triggered by extracellular EBI3. However, little is known about intracellular EBI3 function. In the current study, we report that EBI3 production by macrophages is elevated in TB patients. We further demonstrate that increased EBI3 accumulates in virulent M. tb-treated murine macrophages. Eukaryotic translation elongation factor 1-alpha 1 (eEF1A1) binds to intracellular EBI3 to reduce Lys48 (K48)-linked ubiquitination of EBI3, leading to EBI3 accumulation. Moreover, the intracellular EBI3 inhibits caspase-3-mediated apoptosis in M. tb-treated macrophages. Herein, we propose a novel mechanism for accumulating intracellular EBI3 and its regulation of macrophage apoptosis in response to virulent M. tb.

Indexed as

AnimalsApoptosisCase-Control StudiesCaspase 3Cell LineDisease Models, AnimalHost-Pathogen InteractionsHumansLeukocyte CountMacrophagesMiceMice, KnockoutMinor Histocompatibility AntigensMycobacterium tuberculosisPeptide Elongation Factor 1Protein BindingCASP3 protein, humanCaspase 3Ebi3 protein, mouseMinor Histocompatibility AntigensPeptide Elongation Factor 1Receptors, CytokineRNA, Small InterferingapoptosisEBI3eEF1A1macrophageM. tbubiquitination

Identifiers

PMID30753412
PMCPMC6414311
OpenAlexW2913540900

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.